Real and perceived issues involving animal proteins - C. R. Hamilton
May 3, 2002
FAO CORPORATE DOCUMENT REPOSITORY
Title: PROTEIN SOURCES FOR THE ANIMAL FEED INDUSTRY...
C. R. Hamilton
Director
Research and Nutritional Services
Darling International
Incorporated
U.S.A.
THE RENDERING INDUSTRY
The rendering industry has and continues to be
closely integrated with animal and meat production in countries where these
industries are well established. On a global perspective, rendering provides an
important service to society and the animal feeding industries by processing
approximately 60 million tonnes per year of animal by-products derived from the
meat and animal production industries. During slaughter and processing, between
33 and 43 percent by weight of the live animal is removed and discarded as
inedible waste. These materials, which include fat trim, meat, viscera, bone,
blood and feathers are collected and processed by the rendering industry to
produce high quality fats and proteins that have traditionally been used in the
animal feed and oleochemical industries around the world. Without the rendering
industry, the accumulation of unprocessed animal byproducts would impede the
meat industries and pose a serious potential hazard to animal and human
health.
One definition of rendering is to ‘clarify or
purify by melting’ (heat processing). Unprocessed animal by-products may contain
60 percent or more water (Figure 1).
The primary reasons for using heat when
processing these raw materials are to remove the moisture and facilitate fat
separation. Desiccation significantly reduces the total volume from 60 million
tonnes of raw material to about 8 million tonnes of animal proteins and 8.2
million tonnes of rendered fats. Stored properly, these finished products are
stable for long periods of time. Heat processing also benefits the finished
product customer. The temperatures used (115° to 145° C) are more than
sufficient to kill bacteria, viruses and many other micro-organisms, to produce
an aseptic protein product that is free of potential biohazards and
environmental threats. Done correctly, heat processing also denatures the
proteins slightly, which enhances their digestibility.
Figure 1. Raw material
composition
Modern efficient rendering facilities are
concentrated in countries and regions possessing strong and well-established
animal production industries. Renderers in North America process nearly 25
million tonnes of animal byproducts per year, while those in the European Union
process about 15 million tonnes. Argentina, Australia, Brazil and New Zealand
collectively process another 10 million tonnes of animal byproducts per year.
The total value of finished rendered products, worldwide is estimated to be
between US$6 and US$8 billion per year.
RENDERED PRODUCTS - NUTRITIONAL
VALUE
Animal products include meat and bone meal,
blood meal, poultry by-product meal (poultry meal) and feather meal. These are
all concentrated sources of protein and amino acids and some are also good
sources of vitamins and essential minerals (Table 1).
This makes them important feed ingredients for
livestock, poultry and companion animals in the United States and many other
countries of the world. Meat and bone meal, blood meal, feather meal and poultry
meal are suitable for use in feeds for a wide range of animal species, including
fish and shrimp (Table 2).
As shown in Figure 2, more than two million
tonnes of meat and bone meal and poultry meal combined are used annually by the
United States feed industry alone. Animal proteins have traditionally been
important sources of proteins and other nutrients for livestock and poultry in
the United States and their acceptance in Latin America and Asia has grown
substantially in the past five years. Animal proteins are also used extensively
in pet foods. About 1.5 million tonnes of meat and bone meal and poultry meal is
used by the United States pet food industry each year. The use of non-marine
animal proteins in aquaculture feeds is a relatively new practice, but this
application is expected to continue to grow, especially as competition and
prices for fishmeal increase.
TABLE 1
Nutrient composition of animal
proteinsa
| Item |
Meat & Bone Meal |
Blood Mealb |
Feather Meal |
Poultry Meal |
| Crude protein, % |
50.4 |
88.9 |
81.0 |
60.0 |
| Fat, % |
10.0 |
1.0 |
7.0 |
13.0 |
| Calcium, % |
10.3 |
0.4 |
0.3 |
3.0 |
| Phosphorus, % |
5.1 |
0.3 |
0.5 |
1.7 |
| TMEN, kcal/kg |
2666c |
3625 |
3276 |
3120 |
| Amino Acids |
|
|
|
|
| Methionine, % |
0.7 |
0.6 |
0.6 |
1.0 |
| Cystine, % |
0.7 |
0.5 |
4.3 |
1.0 |
| Lysine, % |
2.6 |
7.1 |
2.3 |
3.1 |
| Threonine, % |
1.7 |
3.2 |
3.8 |
2.2 |
| Isoleucine, % |
1.5 |
1.0 |
3.9 |
2.2 |
| Valine, % |
2.4 |
7.3 |
5.9 |
2.9 |
| Tryptophan, % |
0.3 |
1.3 |
0.6 |
0.4 |
| Arginine, % |
3.3 |
3.6 |
5.6 |
3.9 |
| Histidine, % |
1.0 |
3.5 |
0.9 |
1.1 |
| Leucine, % |
3.3 |
10.5 |
6.9 |
4.0 |
| Phenylalanine, % |
1.8 |
5.7 |
3.9 |
2.3 |
| Tyrosine, % |
1.2 |
2.1 |
2.5 |
1.7 |
| Glycine |
6.7 |
4.6 |
6.1 |
6.2 |
| Serine |
2.2 |
4.3 |
8.5 |
2.7 |
a NRC 1994; b Ring or
flash dried; c Dale, 1997
TABLE 2
Suitability of animal proteins to
supply a portion of the protein in feeds for various animal
species
|
Meal
|
| Specie |
Meat & Bone
|
Blood
|
Feather
|
Poultry
|
| Chickens |
Yes
|
Yes
|
Yes
|
Yes
|
| Turkeys |
Yes
|
Yes
|
Yes
|
Yes
|
| Cattle |
No
|
Yes
|
Yes
|
Yes
|
| Fishb |
Yes
|
Yes
|
Yes
|
Yes
|
| Shrimpb |
Yes
|
?
|
Yes
|
Yes
|
| Dogsc |
Yes
|
Yes
|
Yes
|
Yes
|
a Guaranteed to be free of ruminant
material. b As a partial replacement for fishmeal. c
Approximately 25 to 40% of the dry matter in premium dog foods are animal
by-products.
Some nutritionists underestimate the
digestibility and the nutritional value of animal proteins. This misperception
dates back many years to when poor processing techniques and equipment were used
to render animal by-products. Since that time, new processes, improved equipment
and greater understanding of the effects of time, temperature and processing
methods on amino acid availability have resulted in significant improvements in
the digestibility of animal proteins. Improved understanding as to how best to
incorporate them into commercial formulas and improved formulation procedures
also increased the nutritional value of animal proteins. Data published since
1984 demonstrate that the digestibility of essential amino acids, especially
lysine, threonine, tryptophan and methionine, in meat and bone meal, has
improved (Table 3).
BIOSECURITY AND FINISHED PRODUCT
SAFETY
Biosecurity of food and food related products is
largely perception based on trust and education. Food and feed are derived
directly or indirectly from biological organisms. Natural variation, the
environment, storage conditions, usage and the potential interaction with other
biological organisms (such as micro-organisms) make it impractical to guarantee
food safety in absolute terms. Despite the best efforts on the part of
companies, farmers, regulatory agencies, politicians and others involved in the
food chain, all of the potential risks cannot be alleviated 100 percent of the
time. Therefore, it is necessary to manage these risks using sound scientific
principles and facts. In some recent crisis situations, politics, fear and
supposition have replaced logic and science in risk management
decisions.
Figure 2. Animal protein usage by the United
States' feed industry
TABLE 3
Digestibility of meat and bone
meal since 1984
| Amino Acid |
1984a
|
1989b
|
1990c
|
1992d
|
1995e
|
2001f
|
| Lysine, % |
65
|
70
|
78
|
84
|
94
|
92
|
| Threonine, % |
62
|
64
|
72
|
83
|
92
|
89
|
| Tryptophan, % |
---
|
54
|
65
|
83
|
---
|
86
|
| Methionine, % |
82
|
---
|
86
|
85
|
96
|
92
|
| Cystine, % |
---
|
---
|
---
|
81
|
77
|
76
|
a Jorgensen et al., 1984;
b Knabe et al., 1996; c Batterham et al.,
1990.d Firman, 1992; e Parsons et al., 1997;
f Pearl, 2001b
During the past decade, a number of
safety-related challenges have daunted the rendering industry. These challenges
resulted from perceived rather than proven risks. Public and political
perceptions were influenced by media sensationalism, a general movement of
society away from its agrarian roots, lack of scientific knowledge concerning
bovine spongiform encephalopathy (BSE) and other hazards, inadequate analytical
procedures for routine detection of potential hazards such as dioxins, public
expectations that government and industry assure a safe food supply,
opportunistic marketing strategies and the political agendas of activist
organizations. The Precautionary Principle adopted by the European Union has
served to catalyze these perceptions because in its development and enforcement,
perceived risks and political image frequently overruled science.
The World rendering industry recognizes its role
in assuring food safety and in protecting human and animal health. The rendering
process is an effective method for ensuring biosecurity because processing
conditions and volumes, raw material characteristics and drying create an
unfavorable environment for viruses, bacteria and other micro-organisms to
survive and grow. Rendering is the most logical method for collecting and
processing animal by-products because it possesses the infrastructure to safely
and responsibly recycle these products, allow traceability and produce safe
finished products.
The rendering industry is closely regulated by
the appropriate agencies within the resident region, country or province. In the
United States, State and Federal agencies each routinely inspect rendering
facilities for compliance to applicable regulations and finished product safety
tolerances. Rendering facilities are inspected by the United States Food and
Drug Administration (FDA) for compliance to BSE related regulations. State Feed
Control Officials inspect and test finished products as they enforce quality,
adulteration and feed safety policies.
Rendering industry organizations provide
technical support and education in quality assurance and feed safety. Using
United States based organizations as examples, the Animal Protein Producers
Industry (APPI) administers industry-wide programmes for biosecurity, pathogen
reduction, continuing education and third-party certification for compliance to
BSE related regulations. The Fats and Proteins Research Foundation (FPRF)
solicits and funds industry and university research to address pertinent
biosecurity and nutrient value issues.
Three primary food safety issues dominate
discussions about the safety of feeding animal proteins to animals. These are
Salmonella contamination (bacterial pathogens), BSE and dioxins. Each of
these issues present legitimate concerns and all are known to threaten animal
and human health. However, in each case, the risk of spreading these risks
through finished rendered products is largely perceived rather than factual. The
value of the rendering process as a mechanism to control risks of microbial
pathogens as well as other hazards (with the possible exception of the agent
causing BSE) is illustrated in Table 4, which is based on a report from the
United Kingdom Department of Health (2001).
Salmonella
Salmonella are destroyed by heat when
exposed to temperatures of 55° C for one hour or 60° C for 15 to 20 minutes
(Franco, 1993). Processing temperatures of between 115° C and 145° C are used to
render animal by-products. These temperatures are more than sufficient to kill
Salmonella and other pathogenic bacteria present in raw animal
by-products (Tables 4 and 5). However, Salmonella are opportunistic
organisms and may re-contaminate products after cooking or processing and during
storage, transport and handling. Post process contamination is of concern for
all feed ingredients and not restricted only to animal proteins. Despite this
fact, animal proteins continue to be more closely scrutinized for
Salmonella contamination than other feed ingredients.
Davies and Funk (1999) completed an extensive
review of Salmonella epidemiology and control. They summarized that while
feeds of animal origin receive the most attention as sources of
Salmonella, it is now recognized that feeds of plant origin, such as
soybean meal, are often contaminated with Salmonella. Data showing the
incidence of Salmonella contamination in various feed ingredients in
North America, Europe and the United Kingdom are shown in Table 6. These data
suggest that all feed ingredients may be contaminated with Salmonella.
Brooks (1989) demonstrated that the relative risk of Salmonella
contamination in complete feed is less for animal proteins than for soybean
meal, fishmeal and grain. Even if the Salmonella prevalence in animal
proteins is equal to or exceeds that of other ingredients, animal proteins pose
two- to threefold less risk of contaminating complete feed, because animal
proteins typically have much lower (2 to 5 percent) inclusion rates than other
ingredients (Table 7).
More than 2 200 different serotypes of
Salmonella have been identified and only a few of these cause disease in
humans or animals. Almost all of the Salmonella serotypes that have been
identified in animal proteins are innocuous and do not cause disease (Davies and
Funk, 1999). Furthermore, dried animal proteins do not provide a favorable
environment for Salmonella organisms to proliferate, primarily because
the water activity is too low. Figure 3 illustrates this point.
Salmonella choleraesuis (a human pathogen) remained viable in meat
and bone meal for less than two days after inoculation. In order to limit
Salmonella (or other pathogenic organisms) in meat and other animal
products, it is necessary to control the most important sources of contamination
first. Feed is not the most important contributor to Salmonella
contamination of these products. Data collected from commercial swine production
facilities in the United States suggest that employees, cats, rodents, insects
and environmental factors are much more important Salmonella reservoirs
than feed (Table 8). Drinking water had more than a five-fold greater incidence
of Salmonella than feed.
TABLE 4
Summary of potential health risks
for various methods of handling animal by-products
| Disease/Hazardous Agent |
Exposure of humans to hazards from each handling
method |
| Rendering |
Incineration |
Landfill |
Pyre |
Burial |
Campylobacter, E. coli, Listeria,
Salmonella, Bacillus anthacis, C. botulinum, Leptospira, Mycobacterium
tuberculosis var bovis, Yersinia
|
Low |
Low |
Some |
Low |
High |
| Cryptosporidium, Giardia |
Low |
Low |
Some |
Low |
High |
| Clostridium tetani |
Low |
Low |
Some |
Low |
High |
| Prions for BSE, Scrapie |
Some |
Low |
Some |
Some |
High |
| Methane, CO2 |
Low |
Low |
Some |
Low |
High |
| Fuel-specific chemicals, Metal
salts |
Low |
Low |
Low |
High |
Low |
| Particulates, SO2, NO2,
nitrous particles |
Low |
Some |
Low |
High |
Low |
| PAHs, dioxins |
Low |
Some |
Low |
High |
Low |
| Disinfectants, detergents |
Low |
Low |
Some |
Some |
High |
| Hydrogen sulfide |
Low |
Low |
Some |
Low |
High |
| Radiation |
Low |
Some |
Low |
Some |
Some |
a Adapted from United Kingdom
Department of Health, 2001.
TABLE 5
Efficacy of the United States’
rendering system in the destruction of pathogenic bacteria
| Pathogen |
Raw
Tissueb
|
Post
Processb
|
| Clostridium perfringens |
71.4 %
|
0 %
|
| Listeria species |
76.2 %
|
0 %
|
| L. monocytogenes |
8.3 %
|
0 %
|
| Campylobacter species |
29.8 %
|
0 %
|
| C. jejuni |
20.0 %
|
0 %
|
| Salmonella species |
84.5 %
|
0
%
|
a Trout et al., 2001. Samples
from 17 different rendering facilities taken during the winter and summer.
b Percent of the number of samples found to be positive for pathogens
out of the total samples collected.
TABLE 6
Incidence of Salmonella in
feed ingredients
Ingredient
|
Item
|
Country
|
Netherlandsa
|
Germanyb
|
USAc
|
Canadad
|
United
Kingdome
|
| Animal |
Samples |
2026 |
17 |
101 |
Not reported |
120 |
| Proteins |
% Positive |
6 |
6 |
56 |
20 |
3 |
| Vegetable |
Samples |
1298 |
196 |
50 |
Not reported |
2002 |
| Proteins |
% Positive |
3 |
26 |
36 |
18 |
7 |
| Grains |
Samples |
|
37 |
|
Not reported |
1026 |
| % Positive |
|
3 |
|
5 |
1 |
| Fish Meal |
Samples |
|
|
|
Not reported |
1316 |
| % Positive |
|
|
|
22 |
22 |
a Beumer and Van der Poel, 1997;
b Sreenivas, 1998; c McChesney et al., 1995;
d Canadian Food Inspection Agency, 1999; e Brooks,
1989
TABLE 7
Relative risk of Salmonella
contamination in complete feeda
Ingredient
|
Salmonella
|
Amount in formula
(%)
|
Incidence (%)(+)
|
Risk Factor
|
Grain
|
66.9
|
0.9
|
0.602
|
Soybean meal
|
24.9
|
2.7
|
0.672
|
Fishmeal
|
2.2
|
13.2
|
0.290
|
Meat Meal
|
3.0
|
3.0
|
0.09
|
Fat
|
----
|
----
|
----
|
Vitamin mineral mix
|
----
|
----
|
----
|
a Brooks,
1989
Figure3. Salmonella choleraesius
viability in mammalian bone meal (MBM)a (7 to 25 percent
moisture) and stored at 28.8OC. aSutton et al.
1992
TABLE 8
Reservoirs of Salmonella
contamination on Illinois swine farms.a
| Reservoir |
Number samples
|
Percent
positive
|
| Employee footwear |
93
|
17.2 %
|
| Cats |
22
|
13.6 %
|
| Drinking water |
33
|
12.1 %
|
| Mice/rodents |
59
|
10.2 %
|
| Floor material |
471
|
7.9 %
|
| Flies |
95
|
7.4 %
|
| Feed |
100
|
2.0
%
|
a Weigel et al.
1999.
These data all clearly demonstrate that animal
proteins should not be the primary focus of concern in feeding programs designed
to reduce the incidence of Salmonella. Why then, is Salmonella in
feed ingredients, especially animal proteins, scrutinized so closely? - Because
of perception - not fact. Requiring all animal proteins, or even all feed
ingredients, to be Salmonella free has little impact on overall food
safety without controlling the more important sources of contamination.
Salmonella reduction/prevention is a farm - to - plate issue affecting
all segments of the feed manufacturing, animal production, meat processing and
retail meats industries.
Bovine spongiform encephalopathy
(BSE)
What is BSE (‘Mad Cow Disease’)? ’Mad Cow
Disease’ is an inaccurate term used to describe Bovine Spongiform Encephalopathy
(BSE), because cows do not appear ’mad’ or ’crazy’ when they have the disease.
This was a term coined by the news media in order to gain public attention and
sensationalize the story. BSE is a more appropriate and accurate term to use
when the disease is discussed. BSE is one of several related diseases that
affect a number of different animal species and humans. These diseases are
collectively called transmissible spongiform encephalopathies (TSEs).
BSE is a chronic degenerative disease that
affects the central nervous system of cattle. The only positive cases detected
outside of the United Kingdom and Mainland Europe were reported in Japan in late
2001. The incubation period is thought to be between two and eight years and it
has been associated with a new form of Creutzfeldt-Jakob Disease (CJD) in
humans. CJD has been recognized for many years as a sporadic disease that
affects about 1 person per million. New variant Creutzfeldt-Jakob Disease
(vCJD) differs in etiology and it affects people at a younger
age.
Fortunately, BSE is not easily passed from
animal to animal, so it is not a contagious disease. It also affects specific
tissues in cattle and is confined primarily to the brain, spinal cord and a few
other tissues. Muscle and fat do not appear to be affected by the disease and
are considered to be safe.
Why is BSE a growing concern? BSE is a complex
disease that is poorly understood, even by the scientists who have worked in the
field for many years. At least six different theories are used to explain its
cause and transmission. A complete understanding of the disease is hampered by
the long incubation period (up to 8 years for cattle). As a result, reporters,
activists and some scientists and government officials consider theories and
assumptions as fact. This combined with innuendo and the sensationalism
associated with a possible link between BSE and human disease has created undue
concern and panic among consumers. BSE is also compatible with the anti-meat and
organic food agendas of certain activist groups in the United States and in
Europe. These groups are organized and well funded and have developed focused
media campaigns in order to advance their causes.
No single theory has been proven to explain the
cause of BSE and/or vCJD. Each theory can be supported by
circumstantial, experimental or epidemiological evidence. However, until more is
understood about the disease, theories will continue to be used to explain the
cause. It is clear that abnormal prion proteins are involved in the disease.
However, their role is not completely clear, so it is difficult to determine
whether prion proteins cause disease or are an effect produced by some
unidentified infectious agent or toxin.
Recognize regional differences.
Efficient control and surveillance systems around the world make it possible to
successfully manage the BSE issue. In general, BSE remains a regional disease
and is largely confined to the United Kingdom and Mainland Europe. In the case
of Japan, the cattle found to be positive for BSE were assumed to have
contracted the disease through eating meat and bone meal that was exported from
the United Kingdom or Mainland Europe where BSE had previously occurred.
Therefore, animal proteins from the different countries where BSE has not
existed represent a different risk than countries having the disease. The North
American countries have implemented good BSE prevention efforts. Even though
other transmissible spongiform encephalopathies (TSE), such as Scrapie in sheep
and chronic wasting disease (CWD) in deer and elk exists in these countries,
these diseases have been shown to differ in their etiology from BSE. Australia
and New Zealand are free of these diseases.
Situation in the United States.
The United States differs from Europe. A number of differences between the
United States and Europe, in terms of livestock feeding and rearing practices,
livestock demographics and governmental programmes, exist with respect to BSE
risk assessment.
Sheep and cattle numbers in the United Kingdom
are more concentrated than in the United States (Table 9). The United Kingdom is
roughly the size of the State of Oregon and it has about four times more sheep
than the entire United States. In addition to a dense sheep population, the
United Kingdom also has more than 11 million cattle. As a result, there are
almost 3 sheep for each bovine in the United Kingdom and 12 bovines for every
sheep in the United States. The United Kingdom and the rest of the European
Union have similar livestock demographics.
TABLE 9
Cattle and sheep demographics of
United Kingdom, European Union and United States
| Category |
United Kingdom |
United States |
European Union |
| Cattle and calves (million head) |
11.2
|
99.7
|
82.7
|
| Cattle slaughter (million head) |
2.3
|
35.6
|
27.9
|
| All sheep (million head) |
31.0
|
7.8
|
98.6
|
| Sheep slaughter (million head) |
18.7
|
3.9
|
78.3
|
| Cattle to sheep ratio |
1:2.8
|
12:1
|
1:1.2
|
Because vegetable protein sources are not as
readily available in Europe as they are in the United States, ingredients used
to provide supplemental protein in animal feeds have differed for many years.
Compared to the United States, rendered animal proteins have historically been
used at much higher concentrations in animal feeds in Europe. Further, animal
proteins in Europe were commonly added to veal calf feeds and fed to cattle as
young as two days old. Most United States’ beef production is concentrated in
commercial feedlots where cattle are fed low forage rations consisting primarily
of soy and corn. However, few feedlots exist in Europe and cattle are fed
primarily on grass with protein supplements. Thus, the beef industry in Europe
consists primarily of veal meat and older beef. Because, sheep are the most
common ruminant animal in Europe, rendered animal proteins contained a higher
proportion of sheep material than in the United States. Assuming that all
rendered sheep protein was fed to dairy cows, those in the United Kingdom would
consume 1.54 kg of sheep derived protein per day compared to only 79 grams in
the United States. This comparison is even more dramatic because the US
renderers voluntarily stopped processing sheep material prior to
1995.
Some scientists believe that BSE originated from
Scrapie, a TSE that has been known to affect sheep for more than 300 years.
Given the differences in sheep concentration and production statistics between
the United States and Europe, the risk of BSE occurring in the United States is
markedly lower than in Europe. When differences in feeding practices are also
considered, the level of risk is further decreased.
The ’Triple Firewall’ strategy.
The United States developed a series of ’firewalls’ to prevent BSE from
occurring within its borders. The United States’ risk analysis approach was very
different from that used in Europe, primarily because United States’ officials
recognized from the beginning that zero risk was not attainable. The United
States programme is a progressive and continuously evolving one designed to
proactively prevent the introduction of BSE (import restrictions), prevent
amplification, should the disease ever be introduced into the United States
(ruminant feed ban) and implement an aggressive targeted detection system
(surveillance). All steps were based on science and have been the result of
joint efforts among governmental agencies and all segments of the beef, dairy,
feed and rendering industries (Table 10).
Brain tissue from more than 22 900 cattle were
tested and found to be negative for BSE between 1990 and February of 2002. This
programme has primarily focused on the segment of the cattle population that
represents the greatest risk for BSE. As scientists in Europe have learned more
about the cattle most likely to test positive for the disease, surveillance in
the United States has been adjusted accordingly. The most recent modification to
include ’downer cows’ resulted in a substantial increase in sample submissions.
Target sample numbers for the year 2002 are double the targets for the preceding
year.
The record keeping requirements that rendering
companies and the feed industry are required to comply with also require a high
degree of traceability for animal proteins. Regulated by the FDA, it is possible
to trace finished proteins and fats from collection to use.
Actions by the US rendering
industry. The United States’ rendering industry fully supports BSE
prevention programmes and efforts developed by the United States’ FDA, Animal
and Plant Health Inspection Service (APHIS) and other federal and state
governmental agencies. The rendering industry is committed to achieving 100
percent compliance to the FDA ban (No. 21 CFR 589.2000) which prohibits the
feeding of mammalian proteins (with some specified exemptions) to cattle and
other ruminant animals.
The rendering industry has been actively
involved in programmes to prevent BSE in the United States since before 1995,
when renderers voluntarily stopped rendering sheep material. This was to prevent
any scrapie-infected material from entering the food chain, especially through
feed for ruminant animals.
When the FDA first considered preventative
measures in 1996, renderers and cattle producers voluntarily stopped using meat
and bone meal derived from ruminant animals in cattle feed. This later became
official when the FDA published the rule prohibiting the use of these materials
in feeds intended for cattle and other ruminant animals. The rendering industry
was actively involved in preparing this rule and fully supported it from its
introduction in 1997. The only meat and bone meal permitted for use in ruminant
animal feed in the United States is material that comes from processing plants
that slaughter or process only non-ruminant animals. material is prohibited from
use in feeds for cattle and other ruminant animals.
TABLE 10
Summary of United States BSE
prevention efforts
| Year |
Prevention Programme |
| 1985 |
Imports of British Beef
halted |
| 1986 |
BSE made a legally reportable
disease |
| 1989 |
Ruminant animals from countries with BSE
banned |
| 1990 |
BSE surveillance program
initiated |
| 1990 |
Veterinarian education efforts about BSE
increased |
| 1991 |
Risk assessment conducted (an on-going
process) |
| 1993 |
Surveillance programme
expanded |
| 1996 |
Voluntary ban on use of ruminant derived
proteins in cattle feed initiated |
| 1997 |
FDA ban on use of ruminant derived proteins in
feed for cattle and other ruminants |
| 1997 |
European ruminant animals and products
banned |
| 1998 |
Scrapie eradication program
published |
| 1999 |
Surveillance programme expanded to include
“downer cows” |
| 2000 |
All animal proteins from European Union
banned |
| 2001 |
Harvard Risk Assessment Study to be
completed |
| 2001 |
Risk potential and preventative measures
reassessed - on-going process |
If the raw material cannot be verified to be of
100 percent non-ruminant origin, then the resulting finished. While hazard
analysis critical control point (HACCP) programmes target known hazards that can
be eliminated or controlled through the rendering process, they also include
in-plant enforcement of policies that apply to the acceptance or rejection of
raw material. This provides further assurance that material from suspect cattle
(such as those being tested for BSE through the APHIS surveillance programme),
sheep, goats and other animals susceptible to TSEs are not received and
processed.
The FDA feed ban includes requirements that
finished products are clearly labeled and records of raw material receipts and
finished product sales be kept and made available for inspection by the FDA.
This allows the FDA to verify the source of raw materials and verify compliance
to the feed ban among feed manufacturers, dealers, distributors and end users.
For renderers who process proteins exempted under the feed ban, safeguards to
prevent cross-contamination must be demonstrated in practice and in
writing.
The American Protein Producers Industry (APPI)
recently introduced a certification programme for rendering companies, to verify
compliance to the feed ban, based on inspections by third-party auditors. The
goal is to have 100 percent participation among all rendering companies in the
United States and 100 percent compliance to the feed ban. This program does not
replace FDA inspections, although results are available for FDA review. The
American Feed Ingredient Association (AFIA) developed a similar programme for
commercial feed manufacturers. The American Meat Industry (AMI) has also
developed a programme for cattle producers to certify that the cattle they are
offering for slaughter have been fed in accordance with FDA
regulations.
Harvard Risk Analysis. The United
States Department of Agriculture commissioned the Harvard Center for Risk
Analysis at the Harvard University School of Medicine to evaluate the potential
for BSE to occur in the United States. The ’Harvard Risk Analysis’ was made
public in November 2001 (Cohen et al., 2001). The study concluded that
the United States is highly resistant to any introduction of BSE or similar
disease. Further, BSE is extremely unlikely to become established in this
country because measures taken by agencies of the United States’ government were
and continue to be effective at reducing the spread of BSE. The feed ban
introduced by the FDA in 1997 to prevent amplification of the disease should it
ever occur in the United States, was considered to be one of the most important
safeguards. The full report is available on the USDA web site located at
http://www.aphis.usda.gov/oa/bse/.
Species that animal proteins are derived
from differ in risk. Specie and type of tissue used to produce animal
protein affects the risk from BSE. Neither pork nor poultry derived proteins
have been implicated as potential sources of the BSE agent. Europe is in the
process of classifying its animal by-products in case its total ban on feeding
animal proteins is lifted. Materials derived from non-ruminant animals approved
for human consumption may eventually be available for use in animal feeds. Other
countries are not presently classifying animal by-products, although some
additional actions may occur in the United States as the various regulatory
agencies work to further strengthen BSE prevention efforts, even though
additional regulations are not scientifically warranted.
A number of governmental agencies around the
world are working to develop testing methodologies to assist them in identifying
the type of material from which animal proteins were derived. For example, it is
possible to identify species-specific DNA using polymerase chain reaction (PCR).
Species-specific DNA can be identified even if the DNA is partially degraded. It
is also possible to differentiate skeletal muscle in protein meals, using ELISA.
Detection limits and validation procedures are being completed for these
technologies. As these issues are resolved, acceptable thresholds will be
established by the appropriate regulatory agencies. At present the unit sample
cost is projected to be moderately high. However, as the technology is adopted,
the costs are expected to decrease.
Acceptable testing methodologies to identify
restricted use proteins in feed for cattle and other ruminant animals will make
it simpler to verify compliance to feed bans and restrictions. These regulatory
tools will make it possible to validate that animal proteins are used safely in
feeds, even in countries known to have BSE present. The greatest challenge will
be in establishing uniform threshold limits for the presence of prohibited
materials in these feeds.
Transmission studies. The majority
of experiments designed to study transmission of BSE and other TSEs among
animals of the same species or from specie to specie, used the intra-cranial
route to introduce raw nervous tissue directly into the brain of the test
animals. Oral transmission is assumed to be much less effective because
intestinal absorption followed by transport and concentration of the infectious
agent in the target tissues must occur. Therefore, oral exposure (i.e. via
contaminated feed) is generally assumed to be one hundred thousand-fold less
effective than direct exposure by the intra-cranial route (Schreuder et
al., 1998). Given the potential losses that may occur via oral exposure, a
large number of infectious units must be consumed in order for the disease to
develop. For humans, the oral infectious dose (ID50) is estimated to
be 1013 BSE prion molecules, which is a very large dose compared to
known bacterial and viral pathogens (Gunn, 2001). While heat processing does not
destroy the infectious agent, processing at 134° C for 3 minutes caused a 2.5
log reduction in infectivity (Schreuder et al., 1998). Therefore, the
risk of spreading BSE by feeding fully processed animal proteins is extremely
low.
Pearl (2001a) summarized several oral challenge
studies that are in progress in the United States and in the United Kingdom.
Because BSE has not been found in the United States, BSE challenge studies can
only be conducted in Europe. Scientists in the United States use scrapie and CWD
infected material in their challenge studies.
Chickens orally challenged with
BSE. A 57- month study to determine the susceptibility of chickens to
BSE was conducted in the United Kingdom. Chickens were challenged with BSE
infected brain tissue by intra-cranial, intra-peritoneal and oral (esophageal
tube) routes. No infectivity was found in any of the chicken tissue assayed upon
completion of the study, regardless of the route used to introduce infective
material. These results suggest that BSE is not transmitted to
chickens.
Cattle orally challenged with
Scrapie. An 8-year study conducted in the United States determined the
effects of orally or intra-cranially challenging 34 calves with rendered
proteins and fats from scrapie infected sheep. There was no evidence of oral
transmission at any time during the course of the study. A second experiment,
also in the United States, orally challenged 17 calves with rendered scrapie
positive brain tissue from sheep. All animals were negative for BSE (and
scrapie) after 8 years. However, 9 calves challenged with intra-cerebral
inoculations were positive for a scrapie-like infection.
Cattle orally challenged with chronic
wasting disease. A total of 26 calves were inoculated (oral or
intra-cranial) with brain tissue from CWD infected mule deer in 1997. Three
calves from each challenge group (oral or intra-cranial) were sacrificed in 1999
and found to be negative for disease. The remaining animals are still alive and
all appear healthy.
HAZARD ANALYSIS CRITICAL CONTROL
POINT
Rendering companies in the United States, Europe
and other countries have adopted HACCP programmes as an important component of
their biosecurity and food safety programmes. HACCP programmes require an
evaluation of the entire rendering process, identification of potential hazards
(such as Salmonella), identification of critical points in the process
where the hazard(s) can be controlled and development of procedures to control
these processes and ensure destruction or removal of the hazard. Additional
controls may also be included at various points in the process to assure quality
(QA) of the finished product(s). A generalized HACCP - QA programme for a
typical rendering facility is shown in Figure 4. It is anticipated that the FDA
will require that the US rendering industry use HACCP programmes within the next
two years.
Dioxins
Concern with dioxin increased because of a
clearly criminal act that occurred in Belgium. Prior to this event, most
rendering companies developed and implemented sampling and testing protocols to
ensure that finished fat and animal proteins were not contaminated with
potentially hazardous compounds, such as pesticides and PCB’s. The rendering
process does not produce dioxins, as shown in Table 4. Because of the extremely
expensive nature of analyzing production samples for dioxins, testing protocols
test for PCB’s which are recognized by regulatory agencies all over the world as
indicators of dioxins.
Figure 4. Basic production flow-chart with HACCP
and quality control points
Dioxins can enter rendered products by one of
two methods: (1) the most likely is by accidental or intentional contamination
and (2) the presence of dioxins in animal tissues. Maximum tolerances for PCB’s
already exist. The European Union and the United States FDA are both considering
adoption of maximum tolerance levels for all dioxins. As sensitive and
inexpensive analytical procedures to test for dioxin in the parts per trillion
range are developed, rendering companies will readily adopt the technology to
ensure that finished rendered products are safe from dioxins.
SUMMARY
Animal proteins are an important class of
ingredients for animal nutritionists to use in feed formulas. The United States’
rendering industry produces nutrient rich products that are highly digestible,
do not contain anti-growth factors and are safe to use in livestock, poultry,
pet and aquaculture feeds.
The rendering process kills Salmonella
and other food pathogens, although post process contamination can still occur.
All feed ingredients may be contaminated with Salmonella.
However, reservoirs of Salmonella present
in animal production facilities are a much greater hazard to food safety than
feed ingredients. Until these sources of contamination are controlled, little
benefit to controlling Salmonella prevalence in feed ingredients will be
realized.
Bovine spongiform encephalopathy continues to be
surrounded by myth and misperceptions. If feed-contaminated animal proteins
spread this disease, countries that have never reported an incidence of BSE
represent a much lower risk than those where the disease has occurred. BSE has
never been reported in the United States, despite the presence of a progressive
surveillance programme that began in 1990. The United States complimented
surveillance with import bans and restrictions to prevent introduction of BSE
into the United States. In the event that BSE was ever found in the United
States, the FDA preemptively instituted a ban on the feeding of meat and bone
meal from ruminant animals to cattle and other ruminants to prevent
amplification and spread of the disease. Additionally, the rendering industry
voluntarily stopped processing sheep and goat material and recently introduced
an industry wide programme to verify compliance with the FDA feed ban using
third-party auditors.
Differences between the United States and Europe
in livestock demographics, feeding practices and governmental policies
pertaining to BSE make the occurrence of BSE in the United States unlikely. Oral
transmission via infected feed has not been proven and would require exposure to
an extraordinarily large number of infectious molecules. The sum of all of these
efforts and statistics make it highly unlikely that BSE will occur in the United
States. To date, BSE remains a European phenomenon, with 99 percent of all cases
in the world occurring in the United Kingdom.
Based on current accepted theories, the specific
tissues and animal specie from which the tissues were derived as well as the
country or regions of the world all interact to influence the risk of BSE. As
methodologies are developed that allow identification of the specie and type of
tissue that animal proteins are derived from, it will be much simpler for
governments to regulate the feeding of animal proteins.
The World Rendering Industry supports programmes
to prevent and control BSE. The US Rendering Industry fully complies with the
United States Food and Drug Administration’s ban on feeding certain mammalian
animal proteins to cattle and other ruminants. Rendering companies also support
industry programmes developed to certify compliance with this rule and
participate in the APPI compliance certification programme, using third-party
auditors.
REFERENCES
Batterham, E. S., et al. 1990.
British Journal of Nutrition, 64: 679.
Beumer, H. & Van der Poel, A. F. B.
1997. Feedstuffs, Dec. 29.
Brooks, P. 1989. Technical Service
Publication, National Renderers Association, Inc. Canadian Food Inspection
Agency, 1999.
Cohen, et al. 2001. Report from
the Harvard Center for Risk Analysis, Harvard School of Public
Health.
Dale, N. 1997. Journal of Applied
Poultry Research, 6: 169.
Davies, P. R. & Funk, J. A. 1999.
Proc. 3rd International Symposium on the Epidemiology and Control of
Salmonella in Pork, August 5-7. p. 1-11.
Firman, J. D. 1992. Journal of Applied
Poultry Research, 1: 350.
Franco, D. A. 1993. Proceedings of the
54th Minnesota Nutrition Conference. p. 21-35.
Gunn, M. 2001. Irish Vetinerary
Record, 54(4): 192.
Jorgensen, H., Sauer, W. C. &. Thacker,
P. A. 1984. Journal of Animal Science, 58: 926.
Knabe, D. A. 1996. In: The Original
Recyclers. p. 176-202. APPI, FPRF and NRA.
McChesney, D. G., Kaplan G. & Gardner,
P. 1995. Feedstuffs, Feb. 13. p. 20 & 23.
NRC. 1994. Nutrient Requirements of
Poultry (9th Rev. Ed.). Washington D. C, National Academy
Press.
Parsons, C. M., Castanon, F. & Han,
Y. 1997. Poultry Science, 76: 361.
Pearl, G. G. 2001a. Directors Digest #
308. Fats and Proteins Research Foundation.
Pearl, G. G. 2001b. Proceedings Mid-West
Swine Nutrition Conference. Sept. 5. Indianapolis, IN, USA.
Schreuder, B. E. C., et al. 1998.
Veterinary Record, 142: 474.
Sreenivas., P. T. 1998. Feed
Mixing, 6(5): 8.
Sutton, A. L., Scheidt, A. B. &
Patterson, J. A. 1992. Final Research Report. Fats and Protein Research
Foundation.
Trout, H. F., Schaeffer, D., Kakoma, I. &
Pearl, G. 2001. Directors Digest #312. Fats and Proteins Research
Foundation.
United Kingdom Department of Health.
2001. A rapid qualitative assessment of possible risks to public health from
current foot and mouth disposal options - Main Report. June.
Weigel, R., Barber, D., Isaacson, R. E.,
Bahnson P. B.& Jones, C. J. 1999. Proceedings 3rd
International Symposium on the Epidemiology and Control of Salmonella in
Pork. August 5-7 p. 180-183.
http://www.fao.org/docrep/007/y5019e/y5019e0g.htm
ftp://ftp.fao.org/docrep/fao/007/y5019e/y5019e00.pdf
Real and perceived issues involving animal proteins C. R. Hamilton May 3,
2002, a review of USDA MAD COW DISEASE BSE FEED
FIRST, please see the drastic decrease of mad cow disease in the UK after
the mad cow feed ban went into force ;
SUMMARY OF PASSIVE SURVEILLANCE REPORTS IN GREAT BRITAIN
PASSIVE SURVEILLANCE
SUSPECTS RESTRICTIONS LIFTED DUE TO ALTERNATIVE SLAUGHTER NOT YET SUSPECTS
KNOWN TO HAVE BEEN SLAUGHTERED SUSPECTS WITH OUTCOME SLAUGHTERED SUSPECTS IN
WHICH BSE NOT SLAUGHTERED SUSPECTS IN WHICH BSE PRIVATE SUBMISSIONS IN WHICH
YEAR RESTRICTED DIAGNOSIS NOTIFIED SLAUGHTERED PENDING CONFIRMED CONFIRMED
BSE CONFIRMED
Pre 18.07.88 1142 1 0 980 0 414 727 0
1988 2512 140 0 2372 0 192 2180 4
1989 8443 386 0 8057 0 924 7133 4
1990 17323 682 0 16641 0 2460 14181 0
1991 30003 982 0 29021 0 3995 25026 6
1992 44844 1690 0 43154 0 6474 36680 2
1993 42931 1847 0 41084 0 6714 34370 0
1994 30259 1551 0 28708 0 4765 23943 2
1995 17945 789 0 17156 0 2855 14301 1
1996 10697 547 0 10150 0 2137 8013 3
1997 5604 302 0 5302 0 992 4310 3
1998 4291 260 0 4031 0 852 3179 1
1999 2984 146 0 2838 0 582 2256 2
2000 1870 117 0 1753 0 442 1311 0
2001 1218 66 0 1152 0 371 781 0
2002 877 68 0 809 0 364 445 0
2003 456 43 0 413 0 240 173 0
2004 351 41 0 310 0 228 82 0
2005 186 30 0 156 0 117 39 0
2006 144 26 0 118 0 103 15 0
2007 69 11 0 58 0 51 7 0
2008 39 7 0 32 0 30 2 0
2009 22 7 0 15 0 14 1 0
2010 19 7 0 12 0 12 0 0
2011 11 2 0 9 0 9 0 0
2012 5 2 0 3 0 3 0 0
2013 2 0 0 2 0 2 0 0
2014 2 0 0 2 0 2 0 0
2015 0 0 0 0 0 0 0 0
2016 0 0 0 0 0 0 0 0
Total 223107 9749 0 213358 0 34930 178428 28
Data valid to 31 January 2016
SECOND, what has MAFF...now DEFRA, what have they said about the mad cow
feed ban in the USA in 2012?
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs
of CWD in affected adults are weight loss and behavioural changes that can span
weeks or months (Williams, 2005). In addition, signs might include excessive
salivation, behavioural alterations including a fixed stare and changes in
interaction with other animals in the herd, and an altered stance (Williams,
2005). These signs are indistinguishable from cervids experimentally infected
with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be
introduced into countries with BSE such as GB, for example, infected deer
populations would need to be tested to differentiate if they were infected with
CWD or BSE to minimise the risk of BSE entering the human food-chain via
affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al.,
2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
THIRD, THE USDA FDA TRIPLE MAD COW DISEASE FIREWALL, WAS NOTHING MORE THAN
INK ON PAPER !
now, let’s just for a moment put away the corporate junk science, and let’s
look at recent updated BSE, CWD, Scrapie, TSE Prion sound science, could not
hurt...
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible to Bovine
Spongiform Encephalopathy BSE by Oral Alimentary route
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21
CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from
deer and elk is prohibited for use in feed for ruminant animals. With regards to
feed for non-ruminant animals, under FDA law, CWD positive deer may not be used
for any animal feed or feed ingredients. For elk and deer considered at high
risk for CWD, the FDA recommends that these animals do not enter the animal feed
system.
***However, this recommendation is guidance and not a requirement by law.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
see Singeltary comment ;
Oral transmission and early lymphoid tropism of chronic wasting disease
PrPres in mule deer fawns (Odocoileus hemionus )
These results indicate that CWD PrP res can be detected in lymphoid tissues
draining the alimentary tract within a few weeks after oral exposure to
infectious prions and may reflect the initial pathway of CWD infection in deer.
The rapid infection of deer fawns following exposure by the most plausible
natural route is consistent with the efficient horizontal transmission of CWD in
nature and enables accelerated studies of transmission and pathogenesis in the
native species.
snip...
These results indicate that mule deer fawns develop detectable PrP res
after oral exposure to an inoculum containing CWD prions. In the earliest
post-exposure period, CWD PrPres was traced to the lymphoid tissues draining the
oral and intestinal mucosa (i.e. the retropharyngeal lymph nodes, tonsil, ileal
Peyer's patches and ileocaecal lymph nodes), which probably received the highest
initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie
agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum and
spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of
nine sheep had infectivity in the retropharyngeal lymph node. He concluded that
the tissue distribution suggested primary infection via the gastrointestinal
tract. The tissue distribution of PrPres in the early stages of infection in the
fawns is strikingly similar to that seen in naturally infected sheep with
scrapie. These findings support oral exposure as a natural route of CWD
infection in deer and support oral inoculation as a reasonable exposure route
for experimental studies of CWD.
snip...
Title: Experimental oral transmission of chronic wasting disease (CWD) to
red deer (Cervus elaphus elaphus): early detection and late stage distribution
of protease-resistant protein (PrP-res)
In this study, red deer (Cervus elaphus elaphus) were exposed to the prion
agent by oral administration of brain homogenates from infected Rocky Mountain
elk. Antemortem testing was performed at 7 months post infection and the deer
were euthanized when clinical disease was observed at approximately 18 months
after infection. The abnormal prion protein was assayed by immunohistochemistry,
enzyme linked immunosorbent assay and western blot. Abnormal prion protein was
found in the spinal cord, brainstem, cerebellum, midbrain, thalamus, and
cerebrum in all 4 infected red deer. Most of the lymph nodes throughout the body
were positive for abnormal prion proteins. Abnromal prion protein was observed
in some additional peripheral tissues in some but not all of the deer. In
particular, most areas of the gastrointestinal tract were positive for abnormal
prions, although the salivary glands were rarely positive. This study
demonstrates the potential for oral transmission of chronic wasting disease to
red deer and confirms the usefulness of the current testing methods for post
mortem diagnosis of the disease in this species.
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan.
*** This supports the theory that the importation of BSE contaminated
feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
see page 176 of 201 pages...tss
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many
spontaneous events of mad cow disease $$$
***so 20 cases of atypical BSE in France, compared to the remaining 40
cases in the remaining 12 Countries, divided by the remaining 12 Countries,
about 3+ cases per country, besides Frances 20 cases. you cannot explain this
away with any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
10 years post mad cow feed ban August 1997
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried,
Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5,
2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-
contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-
Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M
CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B
DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal,
JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT
Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral,
BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC
LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall #
V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with
commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross
contaminated with prohibited meat and bone meal and the labeling did not bear
cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
16 years post mad cow feed ban August 1997
2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
17 years post mad cow feed ban August 1997
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR
FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
Monday, October 26, 2015
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
Sunday, April 5, 2015
*** Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed
On-Farm Draft Guidance FDA-2014-D-1180 ***
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral
Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3;
Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6;
Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique,
France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious
Disease control, Sweden; 5Georg August University, Germany; 6German Primate
Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to
contract BSE through contaminated food. For this purpose, BSE brain was titrated
in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose
(MID50) for oral exposure to BSE in a simian model, and, by in doing this, to
assess the risk for humans. Secondly, we aimed at examining the course of the
disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE
brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals
were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already
developed simian vCJD upon oral or intracerebral exposure or are at the onset of
the clinical phase. However, there are differences in the clinical course
between orally and intracerebrally infected animals that may influence the
detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route
using less than 5 g BSE brain homogenate. The difference in the incubation
period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years).
However, there are rapid progressors among orally dosed monkeys that develop
simian v CJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfillment of the study “BSE
in primates“ supported by the EU (QLK1-2002-01096).
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route
using less than 5 g BSE brain homogenate.
look at the table and you'll see that as little as 1 mg (or 0.001 gm)
caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in
primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,
Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Deslys Summary The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease
(vCJD)--is compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to non-human
primates. We gave two macaques a 5 g oral dose of brain homogenate from a
BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months
after exposure, whereas the other remained free of disease at 76 months. On the
basis of these findings and data from other studies, we made a preliminary
estimate of the food exposure risk for man, which provides additional assurance
that existing public health measures can prevent transmission of BSE to
man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)
1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum
used in our study with primates against a bovine brain inoculum with a similar
PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animals
positive/number of animals surviving at the time of clinical onset of disease in
the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log. ic
ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula
Published online January 27, 2005
Calves were challenged by mouth with homogenised brain from confirmed cases
of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were
then left to develop BSE, but were not subjected to the normal stresses that
they might have encountered in a dairy herd. Animals in all four groups
developed BSE. There has been a considerable spread of incubation period in some
of the groups, but it appears as if those in the 1 and 10g challenge groups most
closely fit the picture of incubation periods seen in the epidemic. Experiments
in progress indicate that oral infection can occur in some animals with doses as
low as 0.01g and 0.001g. .........
It is clear that the designing scientists must also have shared Mr
Bradley's surprise at the results because all the dose levels right down to 1
gram triggered infection.
6. It also appears to me that Mr Bradley's answer (that it would take less
than say 100 grams) was probably given with the benefit of hindsight;
particularly if one considers that later in the same answer Mr Bradley expresses
his surprise that it could take as little of 1 gram of brain to cause BSE by the
oral route within the same species. This information did not become available
until the "attack rate" experiment had been completed in 1995/96. This was a
titration experiment designed to ascertain the infective dose. A range of
dosages was used to ensure that the actual result was within both a lower and an
upper limit within the study and the designing scientists would not have
expected all the dose levels to trigger infection. The dose ranges chosen by the
most informed scientists at that time ranged from 1 gram to three times one
hundred grams. It is clear that the designing scientists must have also shared
Mr Bradley's surprise at the results because all the dose levels right down to 1
gram triggered infection.
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease
Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A Technical Abstract: The purpose of this work was to
determine susceptibility of white-tailed deer (WTD) to the agent of sheep
scrapie and to compare the resultant PrPSc to that of the original inoculum and
chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure
(concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All
scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected
in lymphoid tissues at preclinical time points, and deer necropsied after 28
months post-inoculation had clinical signs, spongiform encephalopathy, and
widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile readily passes to deer.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie
offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic
areas, but could occur anywhere that sheep with scrapie and susceptible cervids
cohabitate.
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by intracerebral inoculation with a high attack
rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of scrapie prions to primate after an extended silent
incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary:
The transmissible spongiform encephalopathies (also called prion diseases)
are fatal neurodegenerative diseases that affect animals and humans. The agent
of prion diseases is a misfolded form of the prion protein that is resistant to
breakdown by the host cells. Since all mammals express prion protein on the
surface of various cells such as neurons, all mammals are, in theory, capable of
replicating prion diseases. One example of a prion disease, bovine spongiform
encephalopathy (BSE; also called mad cow disease), has been shown to infect
cattle, sheep, exotic undulates, cats, non-human primates, and humans when the
new host is exposed to feeds or foods contaminated with the disease agent. The
purpose of this study was to test whether non-human primates (cynomologous
macaque) are susceptible to the agent of sheep scrapie. After an incubation
period of approximately 10 years a macaque developed progressive clinical signs
suggestive of neurologic disease. Upon postmortem examination and microscopic
examination of tissues, there was a widespread distribution of lesions
consistent with a transmissible spongiform encephalopathy. This information will
have a scientific impact since it is the first study that demonstrates the
transmission of scrapie to a non-human primate with a close genetic relationship
to humans. This information is especially useful to regulatory officials and
those involved with risk assessment of the potential transmission of animal
prion diseases to humans.
Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion
disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the
past decades, c-BSE's zoonotic potential has been the driving force in
establishing extensive protective measures for animal and human health. In
complement to the recent demonstration that humanized mice are susceptible to
scrapie, we report here the first observation of direct transmission of a
natural classical scrapie isolate to a macaque after a 10-year incubation
period. Neuropathologic examination revealed all of the features of a prion
disease: spongiform change, neuronal loss, and accumulation of PrPres throughout
the CNS.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats
SUMMARY: We are reopening the comment period for our proposed rule that
would revise completely the scrapie regulations, which concern the risk groups
and categories established for individual animals and for flocks, the use of
genetic testing as a means of assigning risk levels to animals, movement
restrictions for animals found to be genetically less susceptible or resistant
to scrapie, and recordkeeping requirements. This action will allow interested
persons additional time to prepare and submit comments.
DATES: The comment period for the proposed rule published on September 10,
2015 (80 FR 54660-54692) is reopened. We will consider all comments that we
receive on or before December 9, 2015. ...
COMMENT SUBMISSION TERRY S. SINGELTARY SR.
WITH regards to Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats, I
kindly submit the following ;
>>>The last major revision of the scrapie regulations occurred on
August 21, 2001, when we published in theFederal Register(66 FR 43964, Docket
No. 97-093-5) a final rule amending part 79 by imposing additional restrictions
on the interstate movement of sheep and goats.<<<
Indeed, much science has changed about the Scrapie TSE prion, including
more science linking Scrapie to humans. sadly, politics, industry, and trade,
have not changed, and those usually trump sound science, as is the case with all
Transmissible Spongiform Encephalopathy TSE Prion disease in livestock producing
animals and the OIE. we can look no further at the legal trading of the Scrapie
TSE prion both typical and atypical of all strains, and CWD all stains. With as
much science of old, and now more new science to back this up, Scrapie of all
types i.e. atypical and typical, BSE all strains, and CWD all strains, should be
regulated in trade as BSE TSE PRION. In fact, I urge APHIS et al and the OIE,
and all trading partners to take heed to the latest science on the TSE prion
disease, all of them, and seriously reconsider the blatant disregards for human
and animal health, all in the name of trade, with the continued relaxing of TSE
Prion trade regulations through the ‘NEGLIGIBLE BSE RISK’ PROGRAM, which was set
up to fail in the first place. If the world does not go back to the ‘BSE RISK
ASSESSMENTS’, enhance, and or change that assessment process to include all TSE
prion disease, i.e. ‘TSE RISK ASSESSMENT’, if we do not do this and if we
continue this farce with OIE and the USDA et al, and the ‘NEGLIGIBLE BSE RISK’
PROGRAM, we will never eradicate the TSE prion aka mad cow type disease, they
will continue to mutate and spread among species of human and animal origin, and
they will continue to kill. ...
please see ;
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
==========================================
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==========================================
.108: Successful oral challenge of adult cattle with classical BSE
Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine
Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge;
Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology
Laboratory; Truro, Nova Scotia, Canada
Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and
food-borne fatal neurological disease which can be orally transmitted to cattle
and humans. Due to the presence of contaminated milk replacer, it is generally
assumed that cattle become infected early in life as calves and then succumb to
disease as adults. Here we challenged three 14 months old cattle per-orally with
100 grams of C-type BSE brain to investigate age-related susceptibility or
resistance. During incubation, the animals were sampled monthly for blood and
feces and subjected to standardized testing to identify changes related to
neurological disease. At 53 months post exposure, progressive signs of central
nervous system disease were observed in these 3 animals, and they were
euthanized. Two of the C-BSE animals tested strongly positive using standard BSE
rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts
S67 PrPsc was not detected using rapid tests for BSE. Subsequent testing
resulted in the detection of pathologic lesion in unusual brain location and
PrPsc detection by PMCA only. Our study demonstrates susceptibility of adult
cattle to oral transmission of classical BSE. We are further examining
explanations for the unusual disease presentation in the third challenged
animal.
***Our study demonstrates susceptibility of adult cattle to oral
transmission of classical BSE. ***
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. ***
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants
and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama
National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and
humans at the molecular level, we investigated the ability of abnormal prion
protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical
scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to
proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding
cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from
transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc
seed from typical and atypical BSE- or typical scrapie-infected brain
homogenates from native host species. In the conventional PMCA, the conversion
of PrPC to PrPres was observed only when the species of PrPC source and PrPSc
seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA
and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested
prion strains. On the other hand, human PrPC was converted by PrPSc from typical
and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports
describing the lack of transmissibility of H-type BSE to ovine and human
transgenic mice, ***our findings suggest that possible transmission risk of
H-type BSE to sheep and human. Bioassay will be required to determine whether
the PMCA products are infectious to these animals.
================
==========================================
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==========================================
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
HD.13: CWD infection in the spleen of humanized transgenic mice
Liuting Qing and Qingzhong Kong Case Western Reserve University; Cleveland,
OH USA
Chronic wasting disease (CWD) is a widespread prion disease in free-ranging
and captive cervid species in North America, and there is evidence suggesting
the existence of multiple CWD strains. The susceptibility of human CNS and
peripheral organs to the various CWD prion strains remains largely unclear.
Current literature suggests that the classical CWD strain is unlikely to infect
human brain, but the potential for peripheral infection by CWD in humans is
unknown. We detected protease-resistant PrPSc in the spleens of a few humanized
transgenic mice that were intracerebrally inoculated with natural CWD isolates,
but PrPSc was not detected in the brains of any of the CWD-inoculated mice. Our
ongoing bioassays in humanized Tg mice indicate that intracerebral challenge
with such PrPSc-positive humanized mouse spleen already led to prion disease in
most animals. These results indicate that the CWD prion may have the potential
to infect human peripheral lymphoid tissues.
From: Terry S. Singeltary Sr.
Sent: Saturday, November 15, 2014 9:29 PM
To: Terry S. Singeltary Sr.
Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984
THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE
R. G. WILL
1984
*** The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT
THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
snip...
85%+ of all human tse prion disease is sporadic CJD.
see what the NIH prion Gods say themselves ;
‘’In the Archives of Neurology you quoted (the abstract of which was
attached to your email), we did not say CWD in humans will present like variant
CJD. That assumption would be wrong.’’
‘’Also, we do not claim that "no-one has ever been infected with prion
disease from eating venison." Our conclusion stating that we found no strong
evidence of CWD transmission to humans in the article you quoted or in any other
forum is limited to the patients we investigated.’’
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
ARS VIRUS AND PRION RESEARCH / Research / Publication #277212
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Susceptibility of cattle to the agent of chronic wasting disease
from elk after intracranial inoculation
Authors
item Greenlee, Justin item Nicholson, Eric item Smith, Jodi item Kunkle,
Robert item Hamir, Amirali
Submitted to: Journal of Veterinary Diagnostic Investigation Publication
Type: Peer Reviewed Journal Publication Acceptance
Date: July 12, 2012
Publication Date: November 1, 2012
Citation: Greenlee, J.J., Nicholson, E.M., Smith, J.D., Kunkle, R.A.,
Hamir, A.N. 2012.
Susceptibility of cattle to the agent of chronic wasting disease from elk
after intracranial inoculation.
Journal of Veterinary Diagnostic Investigation. 24(6):1087-1093.
Interpretive Summary: Chronic Wasting Disease (CWD), a fatal
neurodegenerative disease that occurs in farmed and wild cervids (deer and elk)
of North America, is a transmissible spongiform encephalopathy (TSE). TSEs are
caused by infectious proteins called prions that are resistant to various
methods of decontamination and environmental degradation. Cattle could be
exposed to chronic wasting disease (CWD) by contact with infected farmed or
free-ranging cervids. The purpose of this study was to assess the potential
transmission of CWD from elk to cattle after intracranial inoculation, the most
direct route to test the potential of a host to replicate an isolate of the
prion agent. This study reports that only 2 of 14 calves inoculated with CWD
from elk had clinical signs or evidence of abnormal prion protein accumulation.
These results suggest that cattle are unlikely to be susceptible to CWD if
inoculated by a more natural route. This information could have an impact on
regulatory officials developing plans to reduce or eliminate TSEs and farmers
with concerns about ranging cattle on areas where CWD may be present.
Technical Abstract:
***Cattle could be exposed to the agent of chronic wasting disease (CWD)
through contact with infected farmed or free-ranging cervids or exposure to
contaminated premises. The purpose of this study was to assess the potential for
CWD derived from elk to transmit to cattle after intracranial inoculation.
Calves (n=14) were inoculated with brain homogenate derived from elk with CWD to
determine the potential for transmission and define the clinicopathologic
features of disease.
Cattle were necropsied if clinical signs occurred or at the termination of
experiment (49 months post-inoculation (MPI)).
Clinical signs of poor appetite, weight loss, circling, and bruxism
occurred in two cattle (14%) at 16 and 17 MPI, respectively.
Accumulation of abnormal prion protein (PrP**Sc) in these cattle was
confined to the central nervous system with the most prominent immunoreactivity
in midbrain, brainstem, and hippocampus with lesser immunoreactivity in the
cervical spinal cord.
*** The rate of transmission was lower than in cattle inoculated with CWD
derived from mule deer (38%) or white-tailed deer (86%).
Additional studies are required to fully assess the potential for cattle to
develop CWD through a more natural route of exposure, but a low rate of
transmission after intracranial inoculation suggests that risk of transmission
through other routes is low.
***A critical finding here is that if CWD did transmit to exposed cattle,
currently used diagnostic techniques would detect and differentiate it from
other prion diseases in cattle based on absence of spongiform change, distinct
pattern of PrP**Sc deposition, and unique molecular profile.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Project Number: 5030-32000-103-00 Project Type: Appropriated
Start Date: Oct 01, 2011 End Date: Sep 30, 2016
Objective: 1. Investigate the pathobiology of atypical transmissible
spongiform encephalopathies (TSEs) in natural hosts. A. Investigate the
pathobiology of atypical scrapie. B. Investigate the pathobiology of atypical
bovine spongiform encephalopathy (BSE). 2. Investigate the horizontal
transmission of TSEs. A. Assess the horizontal transmission of sheep scrapie in
the absence of lambing. B. Determine routes of transmission in chronic wasting
disease (CWD) infected premises. C. Assess oral transmission of CWD in reindeer.
3. Investigate determinants of CWD persistence. A. Determine CWD host range
using natural routes of transmission. B. Investigate the pathobiology of CWD.
Approach: The studies will focus on three animal transmissible spongiform
encephalopathy (TSE) agents found in the United States: bovine spongiform
encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease
(CWD) of deer, elk, and moose. The research will address sites of accumulation,
routes of infection, environmental persistence, and ante mortem diagnostics with
an emphasis on controlled conditions and natural routes of infection. Techniques
used will include clinical exams, histopathology, immunohistochemistry and
biochemical analysis of proteins. The enhanced knowledge gained from this work
will help mitigate the potential for unrecognized epidemic expansions of these
diseases in populations of animals that could either directly or indirectly
affect food animals.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2014 Annual Report
1a.Objectives (from AD-416): 1. Investigate the pathobiology of atypical
transmissible spongiform encephalopathies (TSEs) in natural hosts. A.
Investigate the pathobiology of atypical scrapie. B. Investigate the
pathobiology of atypical bovine spongiform encephalopathy (BSE). 2. Investigate
the horizontal transmission of TSEs. A. Assess the horizontal transmission of
sheep scrapie in the absence of lambing. B. Determine routes of transmission in
chronic wasting disease (CWD) infected premises. C. Assess oral transmission of
CWD in reindeer. 3. Investigate determinants of CWD persistence. A. Determine
CWD host range using natural routes of transmission. B. Investigate the
pathobiology of CWD.
1b.Approach (from AD-416): The studies will focus on three animal
transmissible spongiform encephalopathy (TSE) agents found in the United States:
bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic
wasting disease (CWD) of deer, elk, and moose. The research will address sites
of accumulation, routes of infection, environmental persistence, and ante mortem
diagnostics with an emphasis on controlled conditions and natural routes of
infection. Techniques used will include clinical exams, histopathology,
immunohistochemistry and biochemical analysis of proteins. The enhanced
knowledge gained from this work will help mitigate the potential for
unrecognized epidemic expansions of these diseases in populations of animals
that could either directly or indirectly affect food animals.
3.Progress Report: Research efforts directed toward meeting objective 1 of
our project plan, Investigate the pathobiology of atypical transmissible
spongiform encephalopathies (TSEs) in natural hosts, include work in previous
years starting with the inoculation of animals for studies designed to address
the pathobiology of atypical scrapie, atypical bovine spongiform encephalopathy
(BSE), as well as a genetic version of BSE. Animals inoculated with atypical
scrapie have not yet developed disease. Atypical BSE animals have developed
disease and evaluation of the samples is currently underway. Animals inoculated
with a genetic version of BSE have developed disease and the manuscript has been
published (2012). In addition, we have investigated the possibility that
atypical scrapie was present earlier than previously detected in the national
flock by analyzing archived field isolates using methods that were unavailable
at the time of original diagnosis. Sample quality was sufficiently degraded that
modern methods were not suitable for evaluation. In research pertaining to
objective 2, Investigate the horizontal transmission of TSEs, we have initiated
a study to determine if cohousing non-lambing scrapie inoculated sheep is
sufficient to transmit scrapie to neonatal lambs. At this time, scrapie free
ewes have lambed in the presence of scrapie inoculated animals and the lambs are
cohoused with these inoculated animals.
4.Accomplishments 1. Evaluated enzyme immunoassay for rapid identification
of prion disease in livestock. Scrapie of sheep and bovine spongiform
encephalopathy of cattle are diseases that cause damage to the central nervous
system including the retina in the eye. The infectious agent is an abnormal
protein called a prion that has misfolded from its normal state and is resistant
to breakdown by the host cells. Current diagnostic methods require the testing
of brain material, which can be difficult to collect and may lead to
contamination of the environment and exposure of personnel to the infectious
agent. Eyes can be readily collected without opening the skull. ARS researchers
at Ames, Iowa demonstrated that the enzyme immunoassay results using eyes of
negative controls or samples collected from sheep or cattle with clinical signs
were in agreement with approved confirmatory assays (western blot or
immunohistochemistry). These results indicate the retina is a useful tissue for
rapid diagnosis of prion disease in clinically ill sheep and cattle and could be
considered to greatly increase the number of samples submitted for prion disease
diagnosis with a minimal investment of time and limited exposure of personnel to
prion agents.
2. Evaluated E211K cattle as a model for inherited human prion disease.
Prion diseases cause damage to the central nervous system of animals and humans.
The infectious agent is an abnormal protein called a prion that has misfolded
from its normal state and is resistant to breakdown by the host cells and thus
accumulates and damages those cells. Some forms of prion disease are genetic and
can be inherited. Current models of genetic prion disease in humans rely on
mouse models expressing either the human prion protein (E200K) or a combination
of both mouse and human sequences. In addition to being an entirely artificial
system these mouse models have a short lifespan making them a less than ideal
system to study a naturally occurring genetic disorder with a long incubation
time and late onset of disease. Cattle, however, exhibit a number of
similarities to humans with regard to prion disease and perhaps most notable is
the late onset of genetic prion disease. ARS researchers at Ames, Iowa have
produced cattle containing both 1 and 2 chromosome copies of the cattle prion
gene (E211K) and evaluated many aspects of this prion protein from cattle
including protein stability, protein expression levels and ratios, as well as
evidence of oxidative stress. Taken together, these results highlight the
differences between mouse models of genetic prion disease and a naturally
occurring prion disease system in cattle and suggest that cattle will provide a
more relevant understanding of genetic prion disease in humans than do current
rodent models.
Review Publications Smith, J.D., Greenlee, J.J. 2014. Detection of
misfolded prion protein in retina samples of sheep and cattle by use of a
commercially available enzyme immunoassay. American Journal of Veterinary
Research. 75(3):268-272.
Haldar, S., Beveridge, A.J., Wong, J., Singh, A.J., Galimberti, D.,
Borroni, D., Zhu, X., Blevins, J., Greenlee, J., Perry, G., Mukhopadhyay, C.K.,
Schmotzer, C., Singh, N. 2014. A low-molecular-weight ferroxidase is increased
in the CSF of sCJD Cases: CSF ferroxidase and transferrin as diagnostic
biomarkers for sCJD. Antioxidants & Redox Signaling. 19(14):1662-1675.
*** P.126: Successful transmission of chronic wasting disease (CWD) into
mice over-expressing bovine prion protein (TgSB3985) ***
Larisa Cervenakova,1 Christina J Sigurdson,2 Pedro Piccardo,3 Oksana
Yakovleva,1 Irina Vasilyeva,1 Jorge de Castro,1 Paula Saá,1 and Anton Cervenak1
1American Red Cross, Holland Laboratory; Rockville, MD USA; 2University of
California; San Diego, CA USA; 3Lab TSE/OBRR /CBER/FDA; Rockville, MD USA
Keywords: chronic wasting disease, transmission, transgenic mouse, bovine
prion protein
Background. CWD is a disease affecting wild and farmraised cervids in North
America. Epidemiological studies provide no evidence of CWD transmission to
humans. Multiple attempts have failed to infect transgenic mice expressing human
PRNP gene with CWD. The extremely low efficiency of PrPCWD to convert normal
human PrPC in vitro provides additional evidence that transmission of CWD to
humans cannot be easily achieved. However, a concern about the risk of CWD
transmission to humans still exists. This study aimed to establish and
characterize an experimental model of CWD in TgSB3985 mice with the following
attempt of transmission to TgHu mice.
Materials and Methods. TgSB3985 mice and wild-type FVB/ NCrl mice were
intracranially injected with 1% brain homogenate from a CWD-infected Tga20 mouse
(CWD/Tga20). TgSB3985 and TgRM (over-expressing human PrP) were similarly
injected with 5% brain homogenates from CWD-infected white-tailed deer (CWD/WTD)
or elk (CWD/Elk). Animals were observed for clinical signs of neurological
disease and were euthanized when moribund. Brains and spleens were removed from
all mice for PrPCWD detection by Western blotting (WB). A histological analysis
of brains from selected animals was performed: brains were scored for the
severity of spongiform change, astrogliosis, and PrPCWD deposition in ten brain
regions.
Results. Clinical presentation was consistent with TSE. More than 90% of
TgSB3985 and wild-type mice infected with CWD/Tga20, tested positive for PrPres
in the brain but only mice in the latter group carried PrPCWD in their spleens.
We found evidence for co-existence or divergence of two CWD/ Tga20 strains based
on biochemical and histological profiles. In TgSB3985 mice infected with CWD-elk
or CWD-WTD, no animals tested positive for PrPCWD in the brain or in the spleen
by WB. However, on neuropathological examination we found presence of amyloid
plaques that stained positive for PrPCWD in three CWD/WTD- and two
CWD/Elk-infected TgSB3985 mice. The neuropathologic profiles in CWD/WTD- and
CWD/Elkinfected mice were similar but unique as compared to profiles of BSE,
BSE-H or CWD/Tg20 agents propagated in TgSB3985 mice. None of CWD-infected TgRM
mice tested positive for PrPCWD by WB or by immunohistochemical detection.
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
TSS
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET
AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF
THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
CWD to cattle figures CORRECTION
Greetings,
I believe the statement and quote below is incorrect ;
"CWD has been transmitted to cattle after intracerebral inoculation,
although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This
finding raised concerns that CWD prions might be transmitted to cattle grazing
in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight,
revealed abnormal clinical signs, and were euthanatized. Laboratory tests
revealed the presence of a unique pattern of the disease agent in tissues of
these animals. These findings demonstrate that when CWD is directly inoculated
into the brain of cattle, 86% of inoculated cattle develop clinical signs of the
disease.
" although the infection rate was low (4 of 13 animals [Hamir et al.
2001]). "
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Thank you!
Thanks so much for your updates/comments. We intend to publish as rapidly
as possible all updates/comments that contribute substantially to the topic
under discussion.
re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author
Affiliations
1Institute for Neurodegenerative Diseases, University of California, San
Francisco, San Francisco, California 94143 2Department of Neurology, University
of California, San Francisco, San Francisco, California 94143 Correspondence:
stanley@ind.ucsf.edu
Mule deer, white-tailed deer, and elk have been reported to develop CWD. As
the only prion disease identified in free-ranging animals, CWD appears to be far
more communicable than other forms of prion disease. CWD was first described in
1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of
histopathology of the brain. Originally detected in the American West, CWD has
spread across much of North America and has been reported also in South Korea.
In captive populations, up to 90% of mule deer have been reported to be positive
for prions (Williams and Young 1980). The incidence of CWD in cervids living in
the wild has been estimated to be as high as 15% (Miller et al. 2000). The
development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible
to CWD, has enhanced detection of CWD and the estimation of prion titers
(Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces,
even in presymptomatic deer, has been identified as a likely source of infection
for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD
has been transmitted to cattle after intracerebral inoculation, although the
infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding
raised concerns that CWD prions might be transmitted to cattle grazing in
contaminated pastures.
snip...
----- Original Message -----
From: David Colby To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 +
Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor
Department of Chemical Engineering University of Delaware
===========END...TSS==============
SNIP...SEE FULL TEXT ;
Friday, August 14, 2015
*** Susceptibility of cattle to the agent of chronic wasting disease from
elk after intracranial inoculation ***
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
PL1
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
Circulation of prions within dust on a scrapie affected farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben
C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect humans and
animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk
are contagious prion diseases where environmental reservoirs have a direct link
to the transmission of disease. Using protein misfolding cyclic amplification we
demonstrate that scrapie PrPSc can be detected within circulating dusts that are
present on a farm that is naturally contaminated with sheep scrapie. The
presence of infectious scrapie within airborne dusts may represent a possible
route of infection and illustrates the difficulties that may be associated with
the effective decontamination of such scrapie affected premises.
snip...
Discussion
We present biochemical data illustrating the airborne movement of scrapie
containing material within a contaminated farm environment. We were able to
detect scrapie PrPSc within extracts from dusts collected over a 70 day period,
in the absence of any sheep activity. We were also able to detect scrapie PrPSc
within dusts collected within pasture at 30 m but not at 60 m distance away from
the scrapie contaminated buildings, suggesting that the chance of contamination
of pasture by scrapie contaminated dusts decreases with distance from
contaminated farm buildings. PrPSc amplification by sPMCA has been shown to
correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
PPo3-22:
Detection of Environmentally Associated PrPSc on a Farm with Endemic
Scrapie
Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh
Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of
Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories
Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University
of Nottingham; Sutton Bonington, Loughborough UK
Key words: scrapie, evironmental persistence, sPMCA
Ovine scrapie shows considerable horizontal transmission, yet the routes of
transmission and specifically the role of fomites in transmission remain poorly
defined. Here we present biochemical data demonstrating that on a
scrapie-affected sheep farm, scrapie prion contamination is widespread. It was
anticipated at the outset that if prions contaminate the environment that they
would be there at extremely low levels, as such the most sensitive method
available for the detection of PrPSc, serial Protein Misfolding Cyclic
Amplification (sPMCA), was used in this study. We investigated the distribution
of environmental scrapie prions by applying ovine sPMCA to samples taken from a
range of surfaces that were accessible to animals and could be collected by use
of a wetted foam swab. Prion was amplified by sPMCA from a number of these
environmental swab samples including those taken from metal, plastic and wooden
surfaces, both in the indoor and outdoor environment. At the time of sampling
there had been no sheep contact with these areas for at least 20 days prior to
sampling indicating that prions persist for at least this duration in the
environment. These data implicate inanimate objects as environmental reservoirs
of prion infectivity which are likely to contribute to disease transmission.
A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO
CAMELUS) - SPONGIFORM ENCEPHALOPATHY
4.21 Three cases of SE’s with an unknown infectious agent have been
reported in ostriches (Struthio Camellus) in two zoos in north west Germany
(Schoon @ Brunckhorst, 1999, Verh ber Erkeg Zootiere 33:309-314). These birds
showed protracted central nervous symptoms with ataxia, disturbances of balance
and uncoordinated feeding behaviour. The diet of these birds had included
poultry meat meal, some of which came from cattle emergency slaughter
cases.
SE1806
TRANSMISSION STUDIES OF BSE TO DOMESTIC FOWL BY ORAL EXPOSURE TO BRAIN
HOMOGENATE
1 challenged cock bird was necropsied (41 months p.i.) following a period
of ataxia, tremor, limb abduction and other neurological signs.
Histopathological examination failed to reveal any significant lesions of the
central or peripheral nervous systems...
1 other challenged cock bird is also showing ataxia (43 months p.i.).
snip...
94/01.19/7.1
A notification of Spongiform Encephalopathy was introduced in October 1996
in respect of ungulates, poultry and any other animal.
4.23 MAFF have carried out their own transmission experiments with hens. In
these experiments, some of the chickens exposed to the BSE agent showed
neurological symptoms. However MAFF have not so far published details of the
symptoms seen in chickens. Examination of brains from these chickens did not
show the typical pathology seen in other SE’s. 4.24 A farmer in Kent in November
1996 noticed that one of his 20 free range hens, the oldest, aged about 30
months was having difficulty entering its den and appeared frightened and tended
to lose its balance when excited. Having previously experienced BSE cattle on
his farm, he took particular notice of the bird and continued to observe it over
the following weeks. It lost weight, its balance deteriorated and characteristic
tremors developed which were closely associated with the muscles required for
standing. In its attempts to maintain its balance it would claw the ground more
than usual and the ataxia progressively developed in the wings and legs, later
taking a typical form of paralysis with a clumsy involuntary jerky motion.
Violent tremors of the entire body, particularly the legs, became common,
sparked off by the slightest provocation. This is similar to that seen in many
BSE cases where any excitement may result in posterior ataxia, often with
dropping of the pelvis, kicking and a general nervousness. Three other farmers
and a bird breeder from the UK are known to have reported having hens with
similar symptoms. The bird breeder who has been exhibiting his birds for show
purposes for 20 years noticed birds having difficulty getting on to their perch
and holding there for any length of time without falling. Even though the bird
was eating normally, he noticed a weight loss of more than a pound in a bird the
original weight of which was 5 pounds. 4.25 Histological examination of the
brain revealed degenerative pathological changes in hens with a minimal
vacuolation. The presence of PrP immunostaining of the brain sections revealed
PrP-sc positive plaques and this must be regarded as very strong evidence to
demonstrate that the hens had been incubating Spongiform Encephalopathy.
OPINION on : NECROPHAGOUS BIRDS AS POSSIBLE TRANSMITTERS OF TSE/BSE ADOPTED
BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 7-8 NOVEMBER 2002
OPINION
1. Necrophagous birds as possible transmitters of BSE. The SSC considers
that the evaluation of necrophagous birds as possible transmitters of BSE,
should theoretically be approached from a broader perspective of mammals and
birds which prey on, or are carrion eaters (scavengers) of mammalian species.
Thus, carnivorous and omnivorous mammals, birds of prey (vultures, falcons,
eagles, hawks etc.), carrion eating birds (crows, magpies etc.) in general could
be considered possible vectors of transmission and/or spread of TSE infectivity
in the environment. In view also of the occurrence of Chronic Wasting Disease
(CWD) in various deer species it should not be accepted that domestic cattle and
sheep are necessarily the only source of TSE agent exposure for carnivorous
species. While some information is available on the susceptibility of
wild/exotic/zoo animals to natural or experimental infection with certain TSE
agents, nothing is known of the possibility of occurrence of TSE in wild animal
populations, other than among the species of deer affected by CWD in the
USA.
1 The carrion birds are animals whose diet regularly or occasionally
includes the consumption of carcasses, including possibly TSE infected ruminant
carcasses.
snip... skroll down to the bottom ;
Date: Mon, 11 Jun 2001 16:24:51 –0700
Reply-To: Bovine Spongiform Encephalopathy
Sender: Bovine Spongiform Encephalopathy
From: "Terry S. Singeltary Sr." Subject: The Red-Neck Ostrich & TSEs
'THE AUTOPSY'
Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE
sampling FROM HEALTHY USDA CATTLE)
Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform
Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February
2007 to charges of theft of Government funds, mail fraud, and wire fraud. The
owner and his company defrauded the BSE Surveillance Program when they falsified
BSE Surveillance Data Collection Forms and then submitted payment requests to
USDA for the services. In addition to the targeted sample population (those
cattle that were more than 30 months old or had other risk factors for BSE), the
owner submitted to USDA, or caused to be submitted, BSE obex (brain stem)
samples from healthy USDA-inspected cattle. As a result, the owner fraudulently
received approximately $390,000. Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1
include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for
specified risk material (SRM) violations and improved inspection controls over
SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in
future semiannual reports as the relevant audits and investigations are
completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
-MORE Office of the United States Attorney District of Arizona FOR
IMMEDIATE RELEASE For Information Contact Public Affairs February 16, 2007 WYN
HORNBUCKLE Telephone: (602) 514-7625 Cell: (602) 525-2681
CORPORATION AND ITS PRESIDENT PLEAD GUILTY TO DEFRAUDING GOVERNMENT’S MAD
COW DISEASE SURVEILLANCE PROGRAM
PHOENIX -- Farm Fresh Meats, Inc. and Roland Emerson Farabee, 55, of
Maricopa, Arizona, pleaded guilty to stealing $390,000 in government funds, mail
fraud and wire fraud, in federal district court in Phoenix. U.S. Attorney Daniel
Knauss stated, “The integrity of the system that tests for mad cow disease
relies upon the honest cooperation of enterprises like Farm Fresh Meats. Without
that honest cooperation, consumers both in the U.S. and internationally are at
risk. We want to thank the USDA’s Office of Inspector General for their
continuing efforts to safeguard the public health and enforce the law.” Farm
Fresh Meats and Farabee were charged by Information with theft of government
funds, mail fraud and wire fraud. According to the Information, on June 7, 2004,
Farabee, on behalf of Farm Fresh Meats, signed a contract with the U.S.
Department of Agriculture (the “USDA Agreement”) to collect obex samples from
cattle at high risk of mad cow disease (the “Targeted Cattle Population”). The
Targeted Cattle Population consisted of the following cattle: cattle over thirty
months of age; nonambulatory cattle; cattle exhibiting signs of central nervous
system disorders; cattle exhibiting signs of mad cow disease; and dead cattle.
Pursuant to the USDA Agreement, the USDA agreed to pay Farm Fresh Meats $150 per
obex sample for collecting obex samples from cattle within the Targeted Cattle
Population, and submitting the obex samples to a USDA laboratory for mad cow
disease testing. Farm Fresh Meats further agreed to maintain in cold storage the
sampled cattle carcasses and heads until the test results were received by Farm
Fresh Meats.
Evidence uncovered during the government’s investigation established that
Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted
Cattle Population. Specifically, Farm Fresh Meats and Farabee submitted, or
caused to be submitted, obex samples from healthy, USDA inspected cattle, in
order to steal government moneys.
Evidence collected also demonstrated that Farm Fresh Meats and Farabee
failed to maintain cattle carcasses and heads pending test results and falsified
corporate books and records to conceal their malfeasance. Such actions, to the
extent an obex sample tested positive (fortunately, none did), could have
jeopardized the USDA’s ability to identify the diseased animal and pinpoint its
place of origin. On Wednesday, February 14, 2007, Farm Fresh Meats and Farabee
pleaded guilty to stealing government funds and using the mails and wires to
effect the scheme. According to their guilty pleas:
(a) Farm Fresh Meats collected, and Farabee directed others to collect,
obex samples from cattle outside the Targeted Cattle Population, which were not
subject to payment by the USDA;
(b) Farm Fresh Meats 2 and Farabee caused to be submitted payment requests
to the USDA knowing that the requests were based on obex samples that were not
subject to payment under the USDA Agreement;
(c) Farm Fresh Meats completed and submitted, and Farabee directed others
to complete and submit, BSE Surveillance Data Collection Forms to the USDA’s
testing laboratory that were false and misleading;
(d) Farm Fresh Meats completed and submitted, and Farabee directed others
to complete and submit, BSE Surveillance Submission Forms filed with the USDA
that were false and misleading;
(e) Farm Fresh Meats falsified, and Farabee directed others to falsify,
internal Farm Fresh Meats documents to conceal the fact that Farm Fresh Meats
was seeking and obtaining payment from the USDA for obex samples obtained from
cattle outside the Targeted Cattle Population; and
(f) Farm Fresh Meats failed to comply with, and Farabee directed others to
fail to comply with, the USDA Agreement by discarding cattle carcasses and heads
prior to receiving BSE test results. A conviction for theft of government funds
carries a maximum penalty of 10 years imprisonment. Mail fraud and wire fraud
convictions carry a maximum penalty of 20 years imprisonment. Convictions for
the above referenced violations also carry a maximum fine of $250,000 for
individuals and $500,000 for organizations. In determining an actual sentence,
Judge Earl H. Carroll will consult the U.S. Sentencing Guidelines, which provide
appropriate sentencing ranges. The judge, however, is not bound by those
guidelines in determining a sentence.
Sentencing is set before Judge Earl H. Carroll on May 14, 2007. The
investigation in this case was conducted by Assistant Special Agent in Charge
Alejandro Quintero, United States Department of Agriculture, Office of Inspector
General. The prosecution is being handled by Robert Long, Assistant U.S.
Attorney, District of Arizona, Phoenix. CASE NUMBER: CR-07-00160-PHX-EHC RELEASE
NUMBER: 2007-051(Farabee) # # #
WE can only hope that this is a single incident. BUT i have my doubts. I
remember when the infamous TOKEN Purina Feed Mill in Texas was feeding up to 5.5
grams of potentially and probably tainted BANNED RUMINANT feed to cattle, and
the FDA was bragging at the time that the amount of potentially BANNED product
was so little and the cattle were so big ;
"It is important to note that the prohibited material was domestic in
origin (therefore not likely to contain infected material because there is no
evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The
potential risk of BSE to such cattle is therefore exceedingly low, even if the
feed were contaminated."
On Friday, April 30 th , the Food and Drug Administration learned that a
cow with central nervous system symptoms had been killed and shipped to a
processor for rendering into animal protein for use in animal feed. ... FDA's
investigation showed that the animal in question had already been rendered into
"meat and bone meal" (a type of protein animal feed). Over the weekend FDA was
able to track down all the implicated material. That material is being held by
the firm, which is cooperating fully with FDA.
WE now know all that was a lie. WE know that literally Thousands of TONS of
BANNED and most likely tainted product is still going out to commerce. WE know
now and we knew then that .005 to a gram was lethal. WE know that CWD infected
deer and elk, scrapie infected sheep, BSE and BASE infected cattle have all been
rendered and fed back to livestock (including cattle) for human and animal
consumption.
Paul Brown, known and respected TSE scientist, former TSE expert for the
CDC said he had ''absolutely no confidence in USDA tests before one year ago'',
and this was on March 15, 2006 ;
"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the National
Institutes of Health's Laboratory for Central Nervous System Studies and an
expert on mad cow-like diseases, told United Press International. "The question
was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he has "absolutely no confidence in USDA tests before one
year ago" because of the agency's reluctance to retest the Texas cow that
initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven
months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything USDA did before 2005
suspect," Brown said. ...snip...end
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul
Brown is Senior Research Scientist in the Laboratory of Central Nervous System
... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow
issue for some years, and with Linda Detwiler and others sent lengthy detailed
critiques and recommendations to both the USDA and the Canadian Food Agency."
OR, what the Honorable Phyllis Fong of the OIG found ;
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle
Still Remain
Table 1. Animal feed ingredients that are legally used in U.S. animal feeds
Animal
Rendered animal protein from Meat meal, meat meal tankage, meat and bone
meal, poultry meal, animal the slaughter of food by-product meal, dried animal
blood, blood meal, feather meal, egg-shell production animals and other meal,
hydrolyzed whole poultry, hydrolyzed hair, bone marrow, and animal animals
digest from dead, dying, diseased, or disabled animals including deer and elk
Animal waste Dried ruminant waste, dried swine waste, dried poultry litter, and
undried processed animal waste products
snip...
Conclusions
Food-animal production in the United States has changed markedly in the
past century, and these changes have paralleled major changes in animal feed
formulations. While this industrialized system of food-animal production may
result in increased production efficiencies, some of the changes in animal
feeding practices may result in unintended adverse health consequences for
consumers of animal-based food products. Currently, the use of animal feed
ingredients, including rendered animal products, animal waste, antibiotics,
metals, and fats, could result in higher levels of bacteria, antibioticresistant
bacteria, prions, arsenic, and dioxinlike compounds in animals and resulting
animal-based food products intended for human consumption. Subsequent human
health effects among consumers could include increases in bacterial infections
(antibioticresistant and nonresistant) and increases in the risk of developing
chronic (often fatal) diseases such as vCJD. Nevertheless, in spite of the wide
range of potential human health impacts that could result from animal feeding
practices, there are little data collected at the federal or state level
concerning the amounts of specific ingredients that are intentionally included
in U.S. animal feed. In addition, almost no biological or chemical testing is
conducted on complete U.S. animal feeds; insufficient testing is performed on
retail meat products; and human health effects data are not appropriately linked
to this information. These surveillance inadequacies make it difficult to
conduct rigorous epidemiologic studies and risk assessments that could identify
the extent to which specific human health risks are ultimately associated with
animal feeding practices. For example, as noted above, there are insufficient
data to determine whether other human foodborne bacterial illnesses besides
those caused by S. enterica serotype Agona are associated with animal feeding
practices. Likewise, there are insufficient data to determine the percentage of
antibiotic-resistant human bacterial infections that are attributed to the
nontherapeutic use of antibiotics in animal feed. Moreover, little research has
been conducted to determine whether the use of organoarsenicals in animal feed,
which can lead to elevated levels of arsenic in meat products (Lasky et al.
2004), contributes to increases in cancer risk. In order to address these
research gaps, the following principal actions are necessary within the United
States: a) implementation of a nationwide reporting system of the specific
amounts and types of feed ingredients of concern to public health that are
incorporated into animal feed, including antibiotics, arsenicals, rendered
animal products, fats, and animal waste; b) funding and development of robust
surveillance systems that monitor biological, chemical, and other etiologic
agents throughout the animal-based food-production chain “from farm to fork” to
human health outcomes; and c) increased communication and collaboration among
feed professionals, food-animal producers, and veterinary and public health
officials.
REFERENCES...snip...end
Sapkota et al. 668 VOLUME 115 | NUMBER 5 | May 2007 • Environmental Health
Perspectives
NOW, what about the product that is not reported ?
HOW many more Farm Fresh Meats, Inc. and Roland Emerson Farabee's are out
there that submitted bogus samples for the infamous June 2004 ENHANCED BSE MAD
COW COVER-UP, but did not get caught ?
IT was not bad enough to have the USDA et al bungle there own BSE Testing
Protocols up so bad, it took Weybridge and a year of hounding by s o m e, and
finally an act of Congress to finally get that cow confirmed, but once caught
there, i guess the next best thing would be to have bogus BSE testing samples
submitted for testing from healthy USDA cattle, what next ? not to forget about
the other stumbling and staggering Tejas mad cow they rendered without any test
at all, and the other Tejas mad cow that took 7+ months and an act of Congress
to finally get confirmed from Weybridge. my God, even the three stooges, laural
and hardy put all together could have thought up all this. $$$
The beef import forecast for the second quarter was unchanged from last
month’s, despite pressure from higher-than-expected domestic cow slaughter that
has remained high through most of this period. Beef imports into the United
States from Australia, New Zealand, and Uruguay provide additional processing
beef that, along with domestic cow and bull beef, is mixed with 50-percent trim
from fed cattle to make ground beef. Forecast beef exports were raised slightly,
mainly on continued (though gradual) improvements in sales to major Asian
markets. In late May the World Animal Health Organization – known by its French
acronym, OIE – designated the United States as having “controlled risk status”
for bovine spongiform encephalopathy, or BSE. This designation reflects the
OIE’s view that beef produced in the United States is safe for export, since BSE
control measures such as feed bans and removal of specified risk materials
result in negligible risk to consumers. However, the OIE standards are only
guidelines. Individual countries may adopt differing standards, and those
countries that do accept OIE standards must still undertake the bureaucratic
processes to revise their rules and procedures.
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries. The
OIE is not responsible for inaccurate publication of country disease status
based on inaccurate information or changes in epidemiological status or other
significant events that were not promptly reported to then Central
Bureau............
daaa. ...
P.S. Thank You Honorable Phyllis Fong for trying to keep them straight
anyway. ...TSS
Sunday, August 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 – 2009
Saturday, December 12, 2015
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015
Saturday, December 12, 2015
CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
Saturday, December 12, 2015
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
Saturday, February 6, 2016
*** Secretary's Advisory Committee on Animal Health; Meeting [Docket No.
APHIS-2016-0007] Singeltary Submission ***
Friday, February 05, 2016
*** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild ***
Wednesday, January 20, 2016
Exportation of Live Animals, Hatching Eggs, and Animal Germplasm From the
United States [Docket No. APHIS-2012-0049] RIN 0579-AE00 2016-00962
Thursday, January 14, 2016
*** EMERGING ANIMAL DISEASES Actions Needed to Better Position USDA to
Address Future Risks Report to the Chairman, Committee on Energy and Commerce,
House of Representatives December 2015 GAO-16-132
GAO
Friday, January 1, 2016
South Korea Lifts Ban on Beef, Veal Imports From Canada
US CONGRESS, another failed entity...tss
Tuesday, December 29, 2015
*** Congress repeals country-of-origin labeling rule for beef and pork
December 28, 2015 at 2:21am
*** Australian government assessing risk of importing beef from US, Japan
and the Netherlands
Thursday, December 24, 2015
Infectious disease spread is fueled by international trade
Saturday, December 12, 2015
NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE
Prion REPORT December 14, 2015
Thursday, December 17, 2015
Annual report of the Scientific Network on BSE-TSE 2015 EFSA-Q-2015-00738
10 December 2015
Sunday, October 18, 2015
World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research
SSS SHOOT SHOVEL AND SHUT UP !
*** you can find some history of the BSE cases in Canada and Klein’s BSE
SSS policy comment here ;
Tuesday, August 12, 2014
MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST
2014
Saturday, December 12, 2015
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015
Thursday, October 22, 2015
*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk
mad cow disease USDA and what really happened ***
*** Needless conflict ***
Nature 485, 279–280 (17 May 2012) doi:10.1038/485279b
Published online 16 May 2012
Terry S. Singeltary Sr. said:
I kindly wish to submit the following please ;
Comments on technical aspects of the risk assessment were then submitted to
FSIS.
Comments were received from Food and Water Watch, Food Animal Concerns
Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S.
Singeltary.
This document provides itemized replies to the public comments received on
the 2005 updated Harvard BSE risk assessment. Please bear the following points
in mind:
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)
Page 1 of 98
FSIS, USDA, REPLY TO SINGELTARY
Singeltary to APHIS FDA USDA et al ;
Evidence for human transmission of amyloid-β pathology and cerebral amyloid
angiopathy
07 02:27 AM
Terry S. Singeltary Sr. said:
re-Evidence for human transmission of amyloid-β pathology and cerebral
amyloid angiopathy
2015-12-07 02:27 AM
Terry S. Singeltary Sr. said: re-Evidence for human transmission of
amyloid-β pathology and cerebral amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26
April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated
online 11 September 2015 Erratum (October, 2015)
I would kindly like to comment on the Nature Paper, the Lancet reply, and
the newspaper articles.
First, I applaud Nature, the Scientist and Authors of the Nature paper, for
bringing this important finding to the attention of the public domain, and the
media for printing said findings.
Secondly, it seems once again, politics is getting in the way possibly of
more important Transmissible Spongiform Encephalopathy TSE Prion scientific
findings. findings that could have great implications for human health, and
great implications for the medical surgical arena. but apparently, the
government peer review process, of the peer review science, tries to intervene
again to water down said disturbing findings.
where have we all heard this before? it’s been well documented via the BSE
Inquiry. have they not learned a lesson from the last time?
we have seen this time and time again in England (and other Country’s) with
the BSE mad cow TSE Prion debacle.
snip...see full Singeltary Nature comment here;
see Singeltary comments to Plos ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO
PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have
recognised the public sensitivity of these findings and intend to report them in
their proper context. 'This hopefully will avoid misunderstanding and possible
distortion by the media to portray the results as having more greater
significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection)
the researchers have demonstrated the transmission of a pathological process
from two cases one of severe Alzheimer's disease the other of
Gerstmann-Straussler disease to marmosets. However they have not demonstrated
the transmission of either clinical condition as the "animals were behaving
normally when killed". As the report emphasises the unanswered question is
whether the disease condition would have revealed itself if the marmosets had
lived longer. They are planning further research to see if the conditions, as
opposed to the partial pathological process, is transmissible.
what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of
things highly unusual. However it could be argued that the results reveal a
potential risk, in that brain tissue from these two patients has been shown to
transmit a pathological process. Should therefore brain tissue from such cases
be regarded as potentially infective? Pathologists, morticians, neuro surgeons
and those assisting at neuro surgical procedures and others coming into contact
with "raw" human brain tissue could in theory be at risk. However, on a priori
grounds given the highly specific route of transmission in these experiments
that risk must be negligible if the usual precautions for handling brain tissue
are observed.
1
92/11.4/1.1
BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent
the GSS case demonstrates little more than the transmission of BSE to a pig by
intra-cerebral injection. If other prion diseases can be transmitted in this way
it is little surprise that some pathological findings observed in GSS were also
transmissible to a marmoset. But the transmission of features of Alzheimer's
pathology is a different matter, given the much greater frequency of this
disease and raises the unanswered question whether some cases are the result of
a transmissible prion. The only tenable public line will be that "more research
is required’’ before that hypothesis could be evaluated. The possibility on a
transmissible prion remains open. In the meantime MRC needs carefully to
consider the range and sequence of studies needed to follow through from the
preliminary observations in these two cases. Not a particularly comfortable
message, but until we know more about the causation of Alzheimer's disease the
total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH
832 llllYc!eS 2 92/11.4/1.2
>>> The only tenable public line will be that "more research is
required’’ <<<
>>> possibility on a transmissible prion remains
open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is
"more research is required’’ enough time for evaluation ?
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Sunday, November 22, 2015
*** Effect of heating on the stability of amyloid A (AA) fibrils and the
intra- and cross-species transmission of AA amyloidosis Abstract
Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by
extracellular deposition of AA fibrils. AA fibrils are found in several tissues
from food animals with AA amyloidosis. For hygienic purposes, heating is widely
used to inactivate microbes in food, but it is uncertain whether heating is
sufficient to inactivate AA fibrils and prevent intra- or cross-species
transmission. We examined the effect of heating (at 60 °C or 100 °C) and
autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western
blot analysis, transmission electron microscopy (TEM), and mouse model
transmission experiments. TEM revealed that a mixture of AA fibrils and
amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at
135 °C produced large amorphous aggregates. AA fibrils retained antigen
specificity in Western blot analysis when heated at 100 °C or autoclaved at 121
°C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and
bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly
stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA
fibrils at 121 °C or 135 °C significantly decreased amyloid deposition.
Moreover, amyloid deposition in mice injected with murine AA fibrils was more
severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils
autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These
results suggest that AA fibrils are relatively heat stable and that similar to
prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA
fibrils. These findings may contribute to the prevention of AA fibril
transmission through food materials to different animals and especially to
humans.
Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD
54.00
*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery ***
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological
Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a
middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.
the warning shots fired over the bow of the boat that were never heard ;
PITUITARY EXTRACT
This was used to help cows super ovulate. This tissue was considered to be
of greatest risk of containing BSE and consequently transmitting the disease...
NON-LICENSED HUMAN TISSUE DEVICES WERE NOT COMMERCIALLY AVAILABLE
snip...
I was quite prepared to believe in unofficial pituitary hormones, also in
the 1970's, whether as described by Dr. Little, or in other circumstances, for
animal use.
snip...
The fact that there were jars of pituitaries (or extract) around on shelves
is attested by the still potent 1943 pituitaries, described in Stockell Hartree
et al. (J/RF/17/291) which had come from the lab. at Mill Hill. Having taken the
trouble to collect them, they were not lightly thrown out...
3. The extraction is from a pool of pituitary glands collected from
abbatoirs and the process used is unlikely to have any effect on the BSE agent.
Hormones extracted from human pituitary glands have been responsible for a small
number of Creutzfeldt Jacob disease in man.
SEE LOOPHOLE ;
SEE LOOPHOLE SHOULD BE CLOSED ;
snip...see at bottom ;
Friday, January 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type
prion disease, what it ???
Tuesday, August 4, 2015
*** FDA U.S. Measures to Protect Against BSE ***
*** now, from all the consumption and exposure above, now think iatrogenic
cjd tse prion at a hospital near you, what if?
Thursday, August 13, 2015
Iatrogenic CJD due to pituitary-derived growth hormone with genetically
determined incubation times of up to 40 years
Monday, August 17, 2015
*** FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS
*** I told Olympus 15 years ago about these risk factors from endoscopy
equipment, disinfection, even spoke with the Doctor at Olympus, this was back in
1999. I tried to tell them that they were exposing patients to dangerous
pathogens such as the CJD TSE prion, because they could not properly clean them.
even presented my concern to a peer review journal GUT, that was going to
publish, but then it was pulled by Professor Michael Farthing et al... see ;
Thursday, September 10, 2015
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory
Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015
Thursday, January 14, 2016
Preventable Tragedies: Superbugs and How Ineffective Monitoring of Medical
Device Safety Fails Patients REPORT
how can it be, HOW CAN IT BE $$$ not a word about CJD GSS FFI VPSPR TSE
Prions that I saw...absolutely crazy, WE ARE MISSING THE BIGGER PICTURE!
how many victims that will never be reported ???
Saturday, January 16, 2016
Revised Preventive Measures to Reduce the Possible Risk of Transmission of
Creutzfeldt-Jakob Disease and Variant Creutzfeldt-Jakob Disease by Blood and
Blood Products Guidance for Industry
Saturday, February 13, 2016
The Risk of Prion Infection through Bovine Grafting Materials in dentistry
Monday, February 15, 2016
Distinctive properties of plaque-type dura mater graft-associated
Creutzfeldt–Jakob disease in cell-protein misfolding cyclic amplification
The Pathological Protein:
Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases
Philip Yam
''Answering critics like Terry Singeltary, who feels that the US
undercounts CJD, Schonberger _conceded_ that the current surveillance system has
errors but stated that most of the errors will be confined to the older
population''....end
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment
on the CDC's attempts to monitor the occurrence of emerging forms of CJD.
Asante, Collinge et al [1] have reported that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD
and all human TSEs are not reportable nationally. CJD and all human TSEs must be
made reportable in every state and internationally. I hope that the CDC does not
continue to expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in the USA
in both animal and man. CWD in deer/elk is spreading rapidly and CWD does
transmit to mink, ferret, cattle, and squirrel monkey by intracerebral
inoculation. With the known incubation periods in other TSEs, oral transmission
studies of CWD may take much longer. Every victim/family of CJD/TSEs should be
asked about route and source of this agent. To prolong this will only spread the
agent and needlessly expose others. In light of the findings of Asante and
Collinge et al, there should be drastic measures to safeguard the medical and
surgical arena from sporadic CJDs and all human TSEs. I only ponder how many
sporadic CJDs in the USA are type 2 PrPSc?
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003
doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
Original
Xavier Bosch
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is
one of a number of people who have remained largely unsatisfied after being told
that a close relative died from a rapidly progressive dementia compatible with
spontaneous Creutzfeldt—Jakob ...
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie?
28 Mar 01
Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number of
campaigners who say that some sCJD, like the variant CJD related to BSE, is
caused by eating meat from infected animals. Their suspicions have focused on
sheep carrying scrapie, a BSE-like disease that is widespread in flocks across
Europe and North America. Now scientists in France have stumbled across new
evidence that adds weight to the campaigners' fears. To their complete surprise,
the researchers found that one strain of scrapie causes the same brain damage in
mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by
some strains of scrapie," says team member Jean-Philippe Deslys of the French
Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses,
south-west of Paris. Hans Kretschmar of the University of Göttingen, who
coordinates CJD surveillance in Germany, is so concerned by the findings that he
now wants to trawl back through past sCJD cases to see if any might have been
caused by eating infected mutton or lamb...
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
Terry S. Singeltary Sr.
